
MMMuM 







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Class V- 

Book i J2- 





Eye-ground in A rterioselerosi 

(After cl e S c 1 1 vv e i n i I z I 



BLOOD-PEESSUEE 



ITS CLINICAL APPLICATIONS 



BY 

GEORGE WILLIAM .\<>KRIS, A.B., M.D. 

ASSISTANT PBOFESSOB OF MEDICINE IN THE INIVKIISITV OF PENNSYLV \\l \ : \ l-li [NG PHYSICIAN 

TO THE PENNSYLVANIA HOSPITAL; ASSISTANT VISITING PHYSICIAN TO THE > MVKKSITY 

HOSPITAL; ki.i.i.mW mi THE COLLEGE Ol PHYS1CIAN8 Ol PHILADELPHIA; 

MEM UK H IT 111 I ; V — •"< ' I A Tic > N ill AMERICA!) PHYSICIANS, ETC. 



THIRD EDITION, TH0R01 GHLY REVISED 



ILLUSTRATED WITH 110 ENGRAVINGS AND 1 COLORED PLATE 




LEA & FEBIGER 

PHILADELPHIA AND NEW YORK 
1917 






^ 



Copyright 
LEA & FEBIGER 

1917 



S+ 



OCT II 1917 



OCLA478971 



DEDICATED 
TO THE MEMORY OF 

FREDERICK A. PACKARD, M.D. 

WHOSE MEDICAL TALENTS AND KINDLY SPIRIT WERE UNTIMELY LOST TO 

THE COMMUNITY OF PHILADELPHIA, IN WHIC LIVED 

AT WHOSE SUGGESTION VND I \Dl.K WHOSE Gl [DANCE 

THE AUTHOR FIRST UNDERTOOK BLOOD-PRESSURE INVESTIGATIONS 

AND TO 

WHOSE SKILL AND SELF-SACRIFICING PROFESSIONAL - 

HE IN A LARGE MEASURE OWES BIS LIFE. 



PREEACE TO THE THIRD EDITION 



The exhaustion of the second edition of this work within a year 
has given opportunity for the inclusion of n considerable amount of 
new material. While this has been introduced throughout the 
hook, particularly important additions have been made in those 
sections dealing with the functional testing of cardiac efficiency, 
with blood-pressure in disease, in the chapter on the Effects of Drugs 
and in the chapter on Physiology. 

The author has continued his endeavor to present the subjecl of 
blood-pressure in a condensed and practical form as definitely as 
the present state of our knowledge permits. Whenever possible a 
summary of the experimental as well as the clinical data available 
for the consideration of a given topic has been included, together 
with references to articles upon which statement- are based. 

x\s in the earlier editions the chapters upon Physiology and upon 
Venous Blood-pressure have been written and revised by Dr. 
J. Harold Austin. The author's thank- arc due to Miss Eleanor 
A. Cantner for valuable assistance in the preparation of the charts 
and drawings. 

G. W. \. 

1530 Locust Street, 
Philadelphia, Pa. 



CONTEXTS. 



< 11 \rn:i; i. 
The Physiology of Blood-pressure 17 

CHAPTER II. 
The [nstrumentai I stimation oi Blood-pressure 61 

CHAPTER 111. 
The Instrumental Estimation o] Blood-pressure (Continued . S7 

(ii \ l' ii;i; i\ . 
Venous Blood-pressure 140 

CB UTF.i; V. 

The Functional Efficiency of the Circulation as Determinable 
by blood-presst re estimation and allied tests 151 

CHAPTER VI. 
Arterial Hypotension 193 

CHAPTER VII. 
Blood-pressure in Acute Infectious Disease 204 

CHAPTER VIII. 
Blood-pressure in Chronic Infectious Disease 222 

CHAPTER IX. 
Exogenous Intoxications 232 



viii cox TEXTS 

CHAPTER X. 
Blood-pressure in Cardiac Disease, Etc. ... .... 240 

CHAPTEB XI. 
Blood-pressure in Arteriosclerosis— Vascular Crises .... 258 

CHAPTER XII. 
Arterial Hypertensive Cardiovascular Disease, Nephritis, Etc. 274 

CHAPTER XIII. 
Tin; Treatment of Arterial Hypertension 310 

CHAPTER XIV. 

Effects of Drugs and Glandular Extracts on Blood-pressure 
(Arranged Alphabetically) 336 

CHAPTER XV. 
Metabolic Diseases and Miscellaneous Conditions 360 

CHAPTER XVI. 
Diseases of the Nervous System 386 

CHAPTER XVII. 
Blood-pressure in Burger's: and Obstetrtcs 394 

CHAPTER XVIII. 

< ►PHTH \i.moi,(m;v 425 



A CLINICAL STUDY OF BLOOD-PRESSURE. 

CHAPTER 1. 
'mi-: PHYSIOLOGY OF BLOOD-PRESSURE. 

By J. II \K< 'I. I) Al -TIN. M.D. 

Definitions. — Blood-pressure is the term used \<> indicate the 
pressure exerted by the Mood at a given point in the circulatory 
system at a given moment. Thus we may speak of intra-auricular, 
intraventricular, arterial, capillary, or venous blood-pressure. When 
not qualified, the term is used to refer to tin' arterial blood-pressure, 
and in man usually to the pressure in the brachial artery. The 
arterial blood-pressure is constantly undergoing rhythmic fluctua- 
tions due to the cardiac systoles. The highest pressure attained 
during one cardiac cycle is called the systolic pressure ami i> attained 
at the moment of the arrival of the crest of the pulse wave. The 
lowest pressure attained during a cardiac cycle is called the diastolic 
press /ire. The difference between these two pressures is called the 
pulse-pressure. Thus, if the systolic pressure be 120 and thediastolic 
90, then the pulse-pressure would be 30. By mean pressure is under- 
stood the average pressure at a given point. The mean pressure 
is not, however, the arithmetical mean between the systolic and 
diastolic pressures, because the pressure may remain for only a 
moment at the systolic level, falling very quickly to near the diastolic 
level and remaining near it throughout the greater part of the 
average cycle. This is illustrated in Fig. 1, in which obviously 
the average pressure lies much nearer to the diastolic than to 
the systolic. 

In addition to the pressure oscillations, dependent upon the cardiac 
cycle and called oscillations of the first order, there are slower oscil- 
lations in the arterial pressure dependent upon the respiratory 
movements. These are called blood-pressure oscillations of the 
second order. Finally, still slower oscillations, usually over ten to 
twenty cardiac cycles, occur. These are due to various factors, 
2 



is 



PHYSIOLOGY OF BLOOD-PRESSURE 



among which rhythmic variations in the activity of the vasocon- 
strictor centre or in the cardiac activity are the most important. 
These constitute the oscillations of the third order. All three types 
of oscillations are shown in the tracings (see Fig. 6). 




Fig. 1. — <S = systolic pressure; D = diastolic pressure; M = mean or 
average pressure. 

The pressure which is exerted by the blood against the vessel 
wall while the current flows unobstructed through the vessel is 
known as the lateral pressure. The pressure exerted by the blood 
against an obstruction in the lumen of the vessel is known as the 
end pressure. The end pressure exceeds the lateral pressure at any 
given point, and the difference is the pressure that is effective in 
producing the blood flow at that point. The accompanying diagram 
(Fig. 2) illustrates the relation between lateral and end pressures. 



-< 



v 



Fig. 2. — Illustrating lateral pressure: 1,2, 3, k, 5, lateral pressure at points along 
outflow tube; h, the difference between lateral pressure and end pressure at any point. 
(From Howell.) 



End pressure in a branch artery is shown to be approximately 
equal to the lateral pressure in the main trunk at the point at 
which the branch takes origin. The method used commonly for 
the measurement of blood-pressure in man shows the end systolic 
pressure in the brachial artery and the lateral diastolic pressure. 1 

'A. K. Cushny: Zentralbl. f. Physiol., Leipsic u. Wien, 1907-8, xxi, 77; N. D. 
BtraschestOi Arch. f. d. ges. Physiol., Bonn, 1900, rxxviii, 1. 



Miri'ffODS OF MEASVh'KMKXT 



19 



Blood-pressure is usually expressed in millimeters (sometimes 
centimeters) of mercury above or below the atmospheric pressure 
at the same point. Thus blood-pressure of L20 is a pressure thai 
will sustain, in addition to the atmospheric pressure al the point, 
the pressure of a vertical column of mercury 120 mm. high. 




Fig. §. — M, mercury manometer; F, float; G, perforated cap; P, recording pen; 
C, cannula for insertion into vessel; w, washout tube, shown in detail at B; R and 
E, for introduction and outflow of magnesium sulphate solution; both are clamped 
off while recording pressures. (From Howell.) 



Methods of Measurement. — The first exact measurements of blood- 
pressure were published by the Rev. Dr. Stephen Hales, an English- 
man, in a little book entitled Statical Essays, in 1733. He measured 
the pressure in the femoral artery of a horse by connecting it with 
a glass tube and noting the height to which the blood rose in this 
tube held vertically. In 1828 Poiseuille applied the mercury 
manometer to the study of blood-pressure, and in 1847 Ludwig' 
invented the recording manometer with moving drum. Ludwig's 



2C PHYSIOLOGY OT BLOOD-PRESSURE 

method is essentially the one used today in physiological experi- 
ments. A manometer is connected by tubing filled with some 
fluid which will inhibit coagulation, such as saturated magnesium 
sulphate solution, with a cannula introduced into the artery. A 
manometer so connected gives a record of the end pressure in the 
artery. 

In physiological work the mean pressure is obtained by con- 
stricting the communication between the manometer and the vessel 
to a small opening. This prevents the transmission of the faster 
1>I l-pressure oscillation to the manometer, and leads to the pro- 
duction of a straight line representing the average or mean pressure. 
In studies upon man the mean pressure cannot thus be directly 
recorded and is, in fact, difficult to determine. All pressure deter- 
mined upon human beings are therefore, as a rule, either systolic or 





I ... i Diagram "f Hiirthle manometer, Tubing from heart or vessel to small 
tambour 7', l>«>th filled with fluid. Movements of tambour magnified by compound 
lever S, and transmitted t<> writing pen. (From Unwell.) 

diastolic pressures. It is the custom of some authors to speak of 
that pressure which is half-way between the systolic and diastolic 
pressures in man as the mean pressure. This seems to us misleading, 
inasmuch as it may in certain cases be considerably above the true 
mean pressure. Dawson 1 has shown that the mean pressure in 
man is usually obtained by adding approximately one-third of the 
pulse pressure to the diastolic pressure. For the measurement of 
the systolic and diastolic pressures in physiological work, Iliirthle 
devised the membrane manometer which is shown in Fig. 1, since 
the inertia of the column of mercury in the mercury manometer 
is too great to give an accurate record of the rapid fluctuations. 
A manometer of still greater value for the recording of the more 

1 British Med. Jour., L906, ii, 996. 



METHODS or Mh'ASI h'h\\Ii:\ T 



L'l 



minute fluctuations in the blood-pressure is thai devised by Frank. 

'This consists of a delicate membrane mi meter to which there i 

attached, instead of the lever, a small mirror, and the fluctuations 
of the manometer are recorded l>\ a beam of lighl reflected from this 
mirror to a moving film. Frank has also established the mathe- 
matical formulae by which it is possible to calculate the efficiency 




Fig. 5. — Maximum-minimum manometer. When cock a is open and b closed, the 
highest pressure attained during the period of record is transmitted to the manometer 
and retained by the maximum valve. When a is closed and b opened, the mercury 
falls to the lowest pressure occurring in the period of record and is retained there by 
the minimum valve. 



of a manometer and to distinguish between the waves which are 
produced within the manometer itself, as artefacts, and those which 
arise in the vessels to which the manometer is applied. All of the 
more recent studies of the minute variations in the blood-pressure 
have been made by means of a manometer based upon the principle 
of Frank. 



22 PHYSIOLOGY OF BLOOD-PRESSURE 

Another method in use in physiological work for the control of the 
membrane manometer is the so-called valve manometer, or maximal- 
minimal manometer. This is illustrated in Fig. 5. By using one 
valve or the other, either the highest or the lowest pressure occur- 
ring within a given interval of time is recorded. The maximal press- 
ure recorded by such a manometer is not, however, identical with 



14-ui i m i i 1 1 1 1 1 i ii ii i i w 1 1 1 1 1 i \\\w i w in i 1 1 1 n i m n 1 1 1 1 n u i 



'vMyvMVVL ^/if^^^v\ v /v^ / *'vvv 



Fig. G. — Diagram illustrating at Bp a typical blood-pressure curve dampened by 
constricting the communication between the artery and the manometer so as to 
reduce the amplitude of the shortest waves. Shortest waves, cardiac; longer waves, 
respiratory: longest waves (three in the tracing), waves of third order. T, time 
record in seconds. (From Howell.) 

the systolic pressure, nor the minimal with the diastolic pressure. 
This may be seen by referring to Fig. 6. The maximal-minimal 
manometer will record the highest or lowest pressure attained over 
a certain period of time, and this is usually long enough to admit 
the occurrence of all three orders of pressure oscillations. It would 
seem desirable, therefore, to use the terms maximal and minirnal 
pressure in this sense. Certain authors, however, have used these 
terms as synonymous with systolic and diastolic pressures respec- 
tively. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 23 

Measurements of the blood-pressure in the smaller arterioles 
and capillaries either in man or in animals must be made by other 
methods, and are described in a later chapter. 

Venous pressure is measured, in physiological work, in the same 
way as the arterial, but usually with a water manometer rather 
than with a mercury manometer. A pressure of 34 cm., II 2 is 
equal to a pressure of 25 mm. Hg. Blood-pressure within the heart 
is measured by introducing an oiled cannula, either through one of 
the vessels or through a puncture wound, into the chamber within 
which the pressure is desired. 

BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE. 

The blood-pressure in an individual varies with the point of the 
cardiovascular system under consideration, its elevation with 
respect to the heart, and with the phase of the heart, whether systole 
or diastole. These variations are indicated in the table below, 
which gives approximate systolic and diastolic pressures in dif- 
ferent parts of the cardiovascular system at the level of the heart 
in man. That the blood-pressure varies greatly in different parts 
of the vascular system has long been known, the marked differ- 
ence in the force of the stream flowing from a cut artery and from 
a cut vein being a striking illustration. 

Approximate Pressure in Cardiovascular Tree of \ Normal Max, Aged 
Twenty Years, at Level of Heart. 

In mm. Hg. 
Systolic. Diastolic. 

Left ventricle to 200 

Aorta 150 to 200 100 to 120 

Brachial artery 105 to 140 80 to 110 

Radial artery 95 to 125 

Arterioles 80 to 95 

Medium capillaries 50 to 60 50 to 60 

Smallest capillaries 20 to 35 20 to 35 

Smallest veins 20 to 30 20 to 30 

Large vein of arm 1 to 15 1 to 15 

Right ventricle 25 to 60 

Pulmonary artery 25 to 60 15 to 25 

This table is extremely diagrammatic and is intended merely to 
emphasize certain facts. It will be noted that the chief fall in 
pressure occurs between the smaller arteries and the capillaries, 
that is, in the arterioles; furthermore, that this affects the systolic 
pressure more than the diastolic, so that under normal conditions 
the pressure in the capillaries shows no pulse wave. When the 
arterioles are widely dilated this fall of pressure, especially of systolic 



24 PHYSIOLOGY OF BLOOD-PRESSURE 

pressure, in them is diminished and an appreciable pulse may 
penetrate into the capillaries, ruder these conditions the systolic 
pressure in the capillaries approaches that in the smaller arteries, 
and the diastolic pressure in the arteries approaches that of the 
capillaries. It will further be noted that any increase in venous 
pressure must promptly elevate the capillary pressure. Indeed, 
the capillary pressure is more readily raised by venous stasis than 
by increased arterial pressure. 

In the recumbent position the lateral pressure throughout the 
entire length of the aorta is very nearly constant. In the upright 
position, however, the pressure at the lower end of the aorta is 
higher than the pressure at the arch, by the weight of the column of 
blood separating the two points; approximately 2 mm. Hg. perinch. 

Dearborn 1 has recently studied in a series of normal individuals, 
varying in age from eleven to thirty-two years, the blood-pressure 
in the brachial artery compared with the pressure in the posterior 
tibial artery, the latter being measured with the patient recumbent 
and the leg either in a horizontal position or in a vertical position 
upward, anil also with the patient standing. The following table 
shows the range of pressures observed in this series and the averages: 

Posterior tibial artery. 
Leg Leg 

Brachial. horizontal. ' Standing. vertically up. 

lie pressures . . 90 to 165 94 to 230 95 to 2S5 45 to 130 

Average .... 116.2 138 154.25 70.8 

In the veins the pressure is largely dependent upon posture, 
/'. e., upon the height of the point measured above or below the right 
auricle. At the right auricle the pressure is probably about to 10 
nun. I Ig., varying with the phase of respiration, and that in the trunk 
is about '1 nun. higher for every inch below the heart; in the lower 
extremities, however, the xenons pressure, while high, is not so 
high as this calculation would indicate (see p. 140). This relation 
leads to some distention of the veins in the lower and dependent 
portions of the body, while the veins of the upper portion of the 
body are but partially filled. 

The Factors that Maintain and Regulate Blood-pressure.— The 

cardiovascular system may be considered from this point of view 

as consisting of six elements. (1) The heart, the source of energy. 

2) The arteries acting as clastic vessels, dilating to receive each 

new ventricular delivery of blood, and contracting to maintain 

i Am. Phys. Educ. Rev., L915, kx, 337. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 25 

during the filling and resting periods of the hearl an even flow 
through the capillaries. (3) The capillaries, the site of active 
functionation of the blood and with the smaller arterioles the chief 
source of the resistance in the circulation. t) The veins which 
with the capillaries serve as a reservoir, maintaining a pi 
just sufficient to fill promptly the relaxing heart for its next systolic 
contraction. (5) The blood itself, the incompressible, inelastic 
medium which fills the cardiovascular system. (6) The lymphatic 
system with its tissue spaces, serous cavities, and lymphatic channels 
filled with lymph, acting as an additional but less promptly avail- 
able reservoir for body fluids. 

The Heart.— The heart is the chief source of the energy that 
maintains the blood-pressure. The factors that affect the heart's 
efficiency to this end are the factors that influence the output of 
blood per minute from the heart. They are as follows: I The 
diastolic filling of the ventricles; this is dependent upon (a) the 
venous pressure, (b) the length of diastole, and (c) the cardiac tunc. 
(2) The completeness of systolic emptying. (3) The uumber of 
beats per minute, or cardiac rate. I h The efficiency of the valves 
of the heart. The cardiac cycle may be divided into two parts: 
(1) systole, or the period of cardiac contraction; (2) diastole, or 
the period of cardiac relaxation and rest. The ventricular systole 
and diastole are each further subdivided. The first one-third or one- 
fourth of the ventricular systole is occupied in raising the pressure 
within the ventricle, from the pressure produced by the auricular 
systole to the diastolic pressure of the pulmonary artery or of the 
aorta. This is the so-called presphygmic period or " anspannungs- 
zeit." 'When this pressure is attained the semilunar valves open 
and, with the propulsion of the blood onward into the aorta, the 
pressure rises in both ventricle and aorta to the systolic pressure. 
This pressure is then maintained in the ventricle almost to the end 
of systole, driving the blood at an even rate out into the aorta and 
into the smaller vessels. With the relaxation at the close of systole 
the pressure in the ventricles falls to zero as the semilunar valves 
close. Diastole now commences. The venous pressure causes the 
tricuspid and mitral valves to open and the blood fills the ventricles 
at a rate dependent upon the venous pressure. The amount of 
distention produced in the ventricle by a given venous pressure is 
determined by the cardiac tone — the greater the tone, the less the 
distention. When this inflow is completed the diastole proper ends 
and the remainder of the cycle is occupied by a period of rest or 
diastasis. 



26 PHYSIOLOGY OF BLOOD-PRESSURE 

With changes in cardiac rate, the duration of both systole and 
diastole are altered, but the former much less than the latter. The 
length of the systole in man, with a pulse rate of about 75 to 95, 
is from 0.3 to 0.38 second. With slow rates that permit time for 
adequate filling of the ventricles Henderson, 1 Bohr 2 and Putter 3 
have found that providing an adequate venous pressure is main- 
tained, the systolic discharge is under normal conditions practically 
a constant quantity for any given individual, and the changes in 
the rate influence only the duration of diastasis. Hence the cardiac 
• •in put per minute under such conditions will be proportional to 
the cardiac rate. With a more accelerated pulse rate, however, 
Henderson has shown that the ventricle has not sufficient time to 
receive its full quota of blood and the diastole is shortened. In 
consequence, the systolic discharge is diminished, and although the 
volume output per minute still increases as the pulse becomes 
more rapid, it falls farther and farther behind proportionally. Hen- 
derson holds to the view that the systolic output of the heart is 
determined entirely by two factors — the cardiac rate, altering the 
duration of the diastole, and the venous pressure. On the other 
hand, Zuntz 4 and Plesch 5 find evidence to support the view that, 
in addition, the heart is capable of varying its output per minute 
independently of the rate and of the venous pressure, as the result 
of direct changes in the cardiac tonus and in the amplitude of the 
cardiac stroke. 

The pressure which is effective in filling the ventricle of the 
heart is not the auricular pressure measured with respect to the 
atmospheric pressure, but is the difference between the intra- 
auricular and the intrathoracic pressures. This pressure difference 
lias been termed by Henderson and Barringer the effective venous 
pressure. If the intra-auricular pressure is plus 10 mm. of water 
and the intrathoracic pressure is minus 40 mm. of water then the 
<Jfeel ire venous pressure will be 50 mm. of water. 

Henderson and Barringer have found that with normal cardiac 
I mi i us the venous pressure necessary to distend the right ventricle 
as rapidly as it relaxes is not more than 50 mm. of water in excess 
of the intrathoracic pressure. This he calls the critical venous 
pressure. 

Wiggers 6 finds, however, that there exists a level of venous press- 

1 Am. Jour. Physiol., 1912 13, xxxi, 288, 352, 399. 
•Skand. Arch. f. Physiol., L909, xxii, 221. 

Ztschr. f. klin. Med., 1911, lxxiii, 342. 
•Ibid., 1912, lxxiv, 347. 
'Ztschr. f. Physiol., 1912, txvi, 90. 
■Circulation in Bealth and Disease, Philadelphia and New York, 1915. 



BLOOD-PRESSURE THROUGH*)! / THE VASCl LAR TREE 27 

ure (40 to 70 mm. of water) which may be regarded rather a a 
relative ^critical pressure, in the sense thai changes in the venous 
pressure above this will modify the cardiac output per heat only to 
a very small extent. There does exist, he believes, an absolutely 
critical venous pressure, which he places at about 150 mm. of water, 
beyond which the heart do longer increases its outpul per beal 
but instead dilates with diminution in the output per beat. Patter- 
son and Starling' have made observations that suggest thai some 
cases of absolu tel '// critical venous pressure exist as high as 200 to 251 I 
mm. of saline. In pathological hearts with an impaired myocardium 
the absolutely critical venous pressure is probably much reduced. 

Studies upon the dog and man have led Henderson to the \ i«-\\ 
that while normally the pressure in the intrathoracic veins ma\ dur- 
ing a very deep inspiration become less than atmospheric, it never 
normally becomes less than 45 mm. of water above the intrathoracic 
pressure and therefore falls scarcely, if at all, below the critical 
pressure. In normal inspiration, the descent of the diaphragm, 1>\ 
compressing the abdominal capillaries and veins, somewhat increase.' 
the venous flow into the thorax. 

In an athlete, panting after a contest, not only the inspiratory 
descent of the diaphragm, but also the powerful expiratory con- 
traction of the abdominal muscles must hasten the venous flow 
from the splanchnic area to the right auricle, and aid in maintain- 
ing the critical venous pressure in spite of the accelerated cardiac 
rate and hence increased cardiac output. It is probable that in 
extreme tachycardia, the shortening of diastole and consequent 
imperfect filling of the ventricle may actually lead to a diminished 
cardiac output per minute. 

Henderson and Prince 1 from a study of the oxygen pulse (the 
oxygen consumption by the body per minute divided by the pulse 
rate) with varying amounts of work, have concluded that the 
systolic discharge of a well-developed man, working hard and with 
a pulse rate of 140 per minute, is not less than 100 c.c. of blood. 

Venous Pressure. — So long as the relative critical venous pressure 
is maintained, the cardiac output per beat is dependent upon the 
duration of diastole. At slow and normal cardiac rates, the diastolic 
filling is complete, but at accelerated rates the filling becomes pro- 
gressively diminished. Inadequate venous pressure reduces the 
cardiac output. On the other hand, in the presence of a weakened 
heart an abnormally high venous pressure probably tends to keep 
the ventricles overdistended, thus predisposing to dilatation. 

1 The Oxygen Pulse and the Systolic Discharge, Am. Jour. Physiol., 1914, xxxv, 106. 



28 PHYSIOLOGY OF BLOOD-PRESSURE 

Cardiac Rate. At slow and moderate rates the cardiac output 
per minute is probably proportional to the cardiac rate. At more 
rapid rates the minute output increases with the pulse rate, but not 
proportionally. At extremely rapid rates imperfect ventricular 
tilling may probably actually diminish the minute output. 

('unlike Tone. -Either unduly diminished cardiac tone, by per- 
mitting dilatation of the ventricles, or unduly increased cardiac 
tone, by interfering with the diastolic filling, impairs the cardiac 
output. 

Stenotic or incompetent valves tend to diminish the cardiac 
output, although this defect is at first compensated by increased 
amplitude of contraction and frequently by increased rate. 

Of these various factors, changes in one may to some extent be 
compensated by changes in another. 

The elevation of venous pressure may possibly be counteracted 
by an increase of cardiac tone. Since Henderson's studies, however, 
support the view that relaxation of the mammalian heart in diastole 
i- caused purely by the venous pressure, for the present the question 
must be left open, whether the cardiac tone can be altered in the 
normal hearl independently of the venous pressure and for the 
purpose of compensating for changes in the latter. Changes in 
cardiac activity can rarely compensate for the diminished venous 
let urn resulting from hemorrhage, from stagnation of the blood 
in widely dilated peripheral vessels (vasomotor shock) or from 
mechanical obstruction to the venous return. The reflex accelera- 
tion of the cardiac rate that results is usually ineffective. 

Ma rev noted that increased blood-pressure is followed by slowing 
of the pulse, and later Kyster and Hooker 1 showed that this is due 
to vagus stimulation occurring reflexly when the blood-pressure 
in the carotids or the aorta is increased, even though changes in the 
cerebral circulation be excluded. The action of the vagus upon the 
he;nt is to diminish the cardiac rate by reducing the activity of the 
"pace-maker," and therefore to decrease the output per minute, 
and when extreme, to reduce the conductivity of the auriculo- 
ventricular bundle, producing partial or complete block. 

Cohn, Rothberger and Winterberg, and Ganter and Zahn have 
all shown independently that the right vagus depresses especially 
the activity of the sinus node, the pace-maker, whereas the left 

vagus depresses more particularly the conductivity of the auriculo- 
ventricular bundle. Apparently there is a similar distribution of the 

1 ZentralbL f. Physiol., Leipsic u. Wien, 1907, x\i, 615. 



BLOOD PRESSURE THROUGHOUT THE VASCULAR TREE 29 

fibers from the right and left stellate ganglia which in their action 
oppose the vagus fibers. 

The amplitude of cardiac contraction is influenced by the 
coronary circulation. Increased How from the coronary vessels 
increases the cardiac contraction, and this effect occurs, in part, 
at least, independently of the increased supply of nutrition to the 
heart muscle. Porter has shown thai increased intraventricular 
pressure, although it tends to decrease the coronary flow, likewise 
excites a contraction of greater amplitude. 

Roy and Adaini 1 have shown, however, l>\ cardiometer studies that 
with increased aortic and hence intraventricular pressure, even 
though the output per minute may he increased, the residual blood 
(that remaining in the ventricles at the end of systole) i> increased 
and the ventricles become more widely dilated during diastole. 
Excessive aortic pressure therefore leads to loss of ventricular tour 
with dilatation and impairment of cardiac efficiency. 

Composition of the Blood. For the maintenance of the activity 
of the mammalian heart the presence of certain nutrient substances 
and certain salts in the blood stream is essential. The blood, or in 
perfusion experiment- the perfused fluid, must contain oxygen, a 
source of energy such as dextrose, and the salts of sodium, calcium, 
and possibly potassium. Concerning the effects of certain substances 
that may be present in normal circulating blood the following 
summary is given by Wiggers: Calcium is absolutely essential; in 
excess it causes an increased tonus. Barium and strontium have 
similar effects. Potassium is not, perhaps, absolutely necessary; 
its influence when in excess is to stop the heart in extreme relaxa- 
tion. The presence of bile slows the cardiac rhythm and augments 
its tonus. Of the extracts from the organs of internal secretion, 
adrenalin increases the rate and amplitude of the perfused heart 
and reduces its tonus, whereas pituitary extract slows the heart, 
decreases its amplitude, and increases its tonus. 

Arteries. — The elasticity of the arteries, by virtue of which they 
dilate during each systole to accommodate the ventricular output 
with only a moderate rise of the pressure within them, and then 
during diastole contract again, forcing a continuous stream through 
the capillaries and maintaining under normal conditions a fair press- 
ure throughout diastole, is a property of the utmost importance. 
Without this elasticity the strain upon the cardiac muscle would be 
enormously increased, as would be the strain during systole upon 

1 British[Med. Jour., 1888, ii, 321. 



30 PHYSIOWGY OF BLOOD-PRESSURE 

the vessel walls. Were the heart pumping into an absolutely rigid 
system, the cardiac systole would be prolonged, the systolic pressure 
enormously increased and the diastolic pressure would fall to zero, 
with a cessation of flow during diastole. The puhe-pressure would 
equal the systolic pressure. Such an extreme condition never 
actually exists, but some approach toward it may be seen in 
individuals with sclerotic arteries in whom often a systolic press- 
ure of 2()0 may be associated with a diastolic pressure of 130; a 
pulse-pressure, therefore, of 70, as contrasted with the normal 
I nilsc-] iressure of about 30. Obviously this exaggeration of the pulse- 
pressure by rigid vessels will be less marked if the cardiac rate be 
increased and the output per beat correspondingly diminished. The 
pulse-pressure is not infrequently looked upon as a rough measure 
of the cardiac activity. This to some extent it is; yet we have just 
seen it is influenced also to a marked degree by the condition of the 
arteries. It has been commonly accepted that this elasticity of the 
arteries, while it results from the tonus of their muscular coats, is 
to be looked upon as a passive elasticity not unlike that of a rubber 
tube. Hasebroek 1 has, however, recently advanced the hypothesis 
that while the dilatation of the arteries is a passive result of the 
injected volume of blood, their contraction is an active muscular 
act and, indeed, an important adjunct to the heart in the main- 
tenance of blood-pressure and blood flow. 

Arterioles, Capillaries, and Veins. — The smaller arterioles together 
with the capillaries constitute the main resistance in the circulation, 
and are chiefly responsible for the proper distribution of the blood 
flow to various organs and tissues, as the relative demands of these 
for blood changes with altering activity. The blood which reaches 
the smaller arterioles al a mean pressure, but little below that in 
the aorta, leaves them at a very low pressure, varying with the 
portion of the body under consideration. Whether this fall of 
pressure occurs chiefly in the small arterioles or in the capillaries 
is a matter of dispute. The capillaries together with the veins of 
i he body serve as a reservoir for the blood. Complete loss of tone 
in these vessels leads to the accumulation in them, particularly in 
the splanchnic region, of practically all the blood in the body. The 
capillary and venous tone is therefore responsible for maintain- 
ing the supply of blood to the right auricle and this, as we have 
already seen in considering the heart, is of the utmost importance 
for the maintenance of cardiac output and of blood-pressure. The 

1 Deutseh. Arch. f. klin. Med.,]l911, cii, 567. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAIt TREE 31 

peripheral resistance is the result of several factors, including the 

viscosity of the blood and the size of the vessels as controlled by the 
vasomotor system and by the extravascular pressure, such as thai 
exerted by the muscles or viscera through which the ves els pass. 

The Vasomotor System. — In this relation it is the capillaries and 
veins of the splanchnic area that are of greatest significance. This 
was shown experimentally by Ludwig and Thin 1 in 1864. These 
vessels alone are capable of containing all the blood of the bodj and 
were they to lose their tone the individual would promptly " hire. I 
to death in his own vessels," as in vasomotor shock. In certain of 
the lower animals the tone of these vessels is relatively low. The 
hutch rabbit can be killed by simply holding it by the ears in the 
vertical position, the splanchnic vessels not having sufficient tone 
to overcome the force of gravity. In the dog manual pressure over 
the abdomen will cause a prompt rise of carotid blood-pressure of 
20 to 30 mm. of mercury due to the forcing of the blood from the 
vessels onward to the right auricle. The regulation of the tone 
of the arterioles, capillaries, and perhaps veins, is the most impor- 
tant factor toward this end. This is brought about by the vaso- 
motor nervous system. The vasomotor system consists of two main 
parts, the vasoconstrictor system and the vasodilator system. 

Vasomotor nerves have been demonstrated anatomically or func- 
tionally, or in both ways in practically all organs of the body. 
Their action is, however, very much more conspicuous in certain 
vessels than in others. In the cerebral, pulmonary, and coronary 
vessels their action is difficult to demonstrate and their presence 
in these vessels was long disputed. 

Johansson 2 observed that the rise in arterial pressure accompany- 
ing the stimulation of the splanchnic nerve, which carries vaso- 
motor fibers to the splanchnic area, does not consist of a single rise 
and fall, but shows two elevations. 

Elliott 3 who investigated this phenomenon in the cat, ascribes 
the second rise to a discharge of suprarenal secretion into the circu- 
lation, inasmuch as the excitation of the splanchnic nerve fails to 
produce this second elevation after the extirpation of the supra- 
renal glands. This hypothesis is further supported by the work of 
von Anrep. 4 

1 Quoted by Howell: Text-book of Physiology, Philadelphia, 1912; Sitz. d. kais. 
Akad. d. Wiss. math, naturw. CI., 1864, xlix, 2, 442. 

2 Arch. f. Anat. u. Phys., 1891, p. 103. 

3 Jour. Physiol., 1912, xliv, 374. 
« Ibid., xlv, 307. 



PHYSIOLOGY OF BLOOD PRESSURE 

The Vasoconstrictor System. The first important experimental 
studies upon this subject wen' those of Claude Bernard. 1 In 1851 
he noted the dilatation of the vessels in the car of the rabbit after 
cutting it- cervical sympathetic nerve on the same side. Later he 
observed that electrical stimulation of the upper end of the cut 
nerve caused constriction of these dilated vessels. Thus was demon- 
strated the existence of vasoconstrictor nerves. 

The vasoconstrictor system consists of a centre in the medulla 
which i- connected with the vessels of the body by nerve paths, each 
consisting of time neurons. In the medulla beneath the middle 
of the fourth ventricle exists the bilateral nerve centre which is 
chiefly responsible for the maintenance of vasomotor tone. This 
centre is continuously in a state of tonic activity which at times 
undergoes rhythmic fluctuations, giving rise to the Traube waves, 
to be described. Porter has recently found evidence against the 
view that both the arterial tonus and the vasomotor reflexes follow- 
ing stimulation of afferent nerves are controlled by the same master 
cells, the so-called vasomotor centre. lie has been able by the use 
of curare in cats to more than double the sciatic and the depressor 
reflex change in blood-pressure, while the arterial tonus is left sub- 
stantially unchanged. Possibly, therefore, we may be compelled 
to recognize two centres, a vasotonic and a vasoreflex centre, related 
but separable. 2 The axons leading; from these medullary cells 
down the conl to end around cells of the anterior horn, from 
the upper thoracic level to the upper lumbar, and constitute, with 
the medullary c||. the first neuron. The axons of the anterior horn 
cells are medullated and constitute the second neuron in the chain, 
the so-called preganglionic fibers. They pass from the cord in the 
white rami communicantes from the first thoracic to the second or 
fourth lumbar segments, and entering the sympathetic chain, have 
one of three destinations. Those destined for the extremities end 
around cells in the sympathetic chain. The non-medullated fibers 
of these sympathetic cells constitute the third neuron, the post- 
. lionic libels. They pass by the gray rami communicantes back 
to the spinal cord and thence accompany the appropriate spinal 
nerves to their destination. The preganglionic fibers destined for 
iln deeper vessels of the head pass through the white rami of the 
first t" ixth thoracic segments and up the sympathetic to the 
superior cer\ leal ganglion. Prom this point the associated postgan- 
glionic fiber are distributed through the carotid and other vascular 

1 Leoona but lee Liquidea de I'organisme, Paris, L859, 
i \m Jour. Physiol., 191 l 15; icxxvi, H8. 



BLOOD-PRESSURE THR0UGH0U1 THE VASCULAR TRE1 33 

plexuses. The preganglionic fillers destined for the vessels of the 
abdominal and pelvic viscera, the mosl important of all in the 
regulation of blood-pressure, pass directly through the sympathetic 
chain and by way of the splanchnic nerves to the celiac, inferior 
mesenteric, or other large prevertebral ganglia. From these gan- 
glia the postganglionic fibers are distributed to the plexuses around 
the abdominal vessels. Section of the first neuron in tins chain, as 
by section of the cervical cord, leads to extreme loss of vascular 
tone with fall in blood-pressure, failure of the circulation, and death. 
If the circulation be, however, artificially maintained alter section 
n!' the cervical cord, the spinal cells, the second neuron-, gradually 
assume a moderate tonic acitivity and restore a very imperfecl 
vascular tone. This may in turn be destroyed l>; destruction of 
the spinal cord. 

Finally, Goltz 1 has shown that even after destruction of the cord, 
some vascular tone may be recovered which musl be attributed to 
tonic activity either of the third postganglionic neuron or of the 
musculature of the vessel wall. Excitation of the vasoconstrictor 
centre with contraction of the peripheral vessels is called forth by 
the stimulation of pressor fibers, which may be demonstrated in 
almost any large nerve containing afferent fibers, but especially in 
the cutaneous nerves. These pressor fibers may be stimulated by 
electricity, by cold applied to the skin, and in other ways. I >epres- 
sion of the centre with diminished contraction of the vessels is 
called forth by stimulation of other afferent fibers, called depressor 
fibers. These likewise may be demonstrated in many of the large 
afferent nerves. Thus, application of warmth to the skin leads to 
local vascular dilatation, the result of stimulation of depressor 
fibers. Sensory stimuli from certain regions, notably the middle 
ear and the testis, gh'e rise, as a rule, to depressor effects. Electric 
stimulation of the central end of the cut sciatic or of the splanchnic 
nerve may lead to either pressor or depressor effects. 

Since mental ivork or especially mental interest leads to a con- 
striction of the bloodvessels with a rise of blood-pressure, it seems 
likely that pressor and probably also depressor fibers pass from the 
cortical centres to the vasoconstrictor centre. Medullary anemia 
and increased C0 2 concentration of the medullary blood are both 
potent stimulants to the vasoconstrictor centre. Many drugs exert 
a direct effect upon this centre. Ludwig and Cyon, 2 in 1S66, demon- 
strated in the rabbit the so-called depressor nerve of the heart. 

i Arch. f. d. gesamt. Physiologie, 1896, lxiv, 397. 

2 Bericht d. sachsisch. Gesellsch. d. Wissensch. math. Phys. CI., 1S66, p. 315. 
3 



34 PHYSIOLOGY OF BLOOD-PRESSURE 

This is an afferent nerve running in the sheath with the vagus, or 
in other species forming a part of the vagus. Stimulation of its 
peripheral cut end is without effect, but of its central end, leads to 
depression of the vasomotor centre and stimulation of the cardio- 
inhibitory centre, tending to lower blood-pressure. It is supposed 
to exert a steadying effect upon blood-pressure and to be stimulated 
mechanically by increase of aortic pressure. The older view that it 
was stimulated chiefly by intraventricular pressure has been ren- 
dered improbable by the work of Eyster and Hooker. 1 Einthoven 2 
has found an impulse passing up this nerve with every cardiac beat. 

The Vasodilator System. — It was likewise Claude Bernard 3 who 
first recognized the existence of vasodilator nerves. He noted that 
stimulation of the peripheral end of the cut chorda tympani nerve 
caused great dilatation of the bloodvessels of the submaxillary gland, 
with increased flow through the afferent vein; this vein in some cases 
actually pulsated. Dilator fibers have been demonstrated in certain 
of the cranial nerves and in the sympathetic chain. The chorda 
tympani conveys such fibers from the facial nerve for distribution 
to the submaxillary and sublingual glands and the anterior two- 
thirds of the tongue. The glossopharyngeal nerve carries such 
fibers to the posterior third of the tongue, the tonsils, pharynx, and 
parotid gland. 

From the cervical sympathetic dilator, fibers pass to the lips, 
gums, palate and skin of the face, passing through the Gasserian 
ganglion and thence with the fifth nerve. From the thoracic sym- 
pathetic dilator, fibers pass through the splanchnic nerves to the 
abdominal viscera. From the first to third sacral segments of the 
cord dilator fibers pass to the hypogastric plexus, whence as the 
nervi erigentes they supply the penis, and when stimulated cause 
erection. The existence of dilator fibers to the limbs, first upheld 
by Goltz, has been rendered uncertain by the work of Bayliss. 4 
Both types of efferent fibers, vasoconstrictor and vasodilator, may 
exist in the same nerve, for example, in the splanchnic. As a rule 
these fibers react to different types of electrical stimulation, the 
dilators responding to weaker and to more slowly interrupted cur- 
rents, responding less promptly, and once having done so, showing 
a more prolonged reaction than do the constrictor fibers. More- 
over, a few days after section of such a nerve the irritability of the 
constrictor fibers is lost, while that of the dilators is still retained. 

There is no evidence that there exists one general vasodilator 

1 Loc. cit. 2 Quoted by Howell. * Loc. eit. 

4 .Jnur. Physiol., 1900, xxvi, 173; ibid., 1902, xxviii, 27G. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 35 

centre associated with the dilator nerves, but rather that there are 
many centres through the cerebrospinal axis for the various areas 
supplied. Probably the vasodilator system is of less significance 
in the regulation of the general blood-pressure, bu1 is concerned in 
local augmentation of blood flow in response to local needs, a., in 
increased glandular or muscular activity. So far as we know there 
is no tonic activity of the vasodilators. How the stimulation of the 
dilator fibers leads to dilatation of the vessels is a subjecl of specu- 
lation. Howell has contended thai it is probably by direcl inhibi- 
tion of the muscles in the vessel walls. 

Chemical Regulation. The possibility of a chemical regulation 
of vascular tone has attracted some attention. Gaskell lias shown 
that acids in low concentration cause vascular dilatation, and in 
this connection the local action of lactic acid and carbon dioxide 
generated during muscular activity has been suggested. 

The idea that a continued pouring of epinephrin from tin' adrenal 
glands into the circulation is a factor in the maintenance of normal 
vascular tone is now questioned. IToskins and McClure 1 have 
obtained no fall in blood-pressure after ligation of the adrenal 
They have also found that an amount of epinephrin in the circula- 
tion sufficient to affect the blood-pressure is enough to cause sup- 
pression of intestinal peristalsis. The various studies tending to 
show by one test or another that there is adrenalin demonstrable in 
the circulating blood have been shown by Stewart, O'Connor, 
Schultz, and Janeway and Park to be based on unreliable methods, 
and as Janeway and Park 2 assert, at the present time there is no 
evidence that epinephrin, in amounts sufficient to produce its phy- 
siological effects upon any hitherto used test objects, exists in the 
circulating blood, with the exception of the blood from the supra- 
renal vein. Cannon's 3 recent work, indicating that after excitement 
in cats there is an increased output of adrenal secretion, suggests 
that this may be a factor in the rise of general arterial pressure inci- 
dent to excitement or exertion. As to the action of other organs of 
internal secretion upon the maintenance or regulation of blood- 
pressure the findings are inconclusive. Extracts of the pituitary 
gland produce on injection a brief fall in blood-pressure, followed by 
a rise. The depressor substance is related to cholin. 4 The pressor 
substance differs somewhat in its effects from that obtained from 
the adrenals. Extracts of various mammalian tissues, thyroid, liver, 

1 Am. Jour. Physiol., 1911-12, xxx, 192; ibid., 1912-13, xxxi, 59. 

2 Jour. Exper. Med., 1912, xvi, 541. 3 Am. Jour. Physiol., 1913, xxxii, 44. 
4 C. J. Wiggers: Am. Jour. Med. Sc, 1911, cxli, 502. 



36 PHYSIOLOGY OF BLOOD-PRESSURE 

pancreas, thymus, testis, bone marrow, the intestine from various 
levels, parathyroid, brain, prostate, ovary, in the hands of most 
observers produce on injection a fall of blood-pressure. 1 This fall 
may be due in some instances to the presence of cholin. A pressor 

substance has been obtained from the kidney, and certain observers 
with some of the above-mentioned organs from certain mammals 
have obtained pressor instead of, or in addition to, depressor effects. 
This action of tissue extracts from such diverse sources is not, 
however, to be understood to mean that these organs are during 
life pouring into the blood stream substances serving to influence 
and regulate blood-pressure. We have no proof that the substance 
extracted from these organs ever pass normally from them into the 
blood stream, nor that they have anything to do with the regulation 
of blood-pressure. 

The Blood and the Lymph. — Within a wide range the tonus of the 
capillaries and veins compensates for changes in the total volume 
of blood. Thus, 2.8 per cent, of the body weight, or about one- 
third of the entire volume of an animal's blood, may be withdrawn 
without any fall in the arterial pressure. Upon the withdrawal of 
a somewhat larger quantity, however, the capillaries and veins no 
longer can maintain an adequate supply to the right auricle. Dimin- 
ution in the cardiac output results and the arterial pressure falls. 

The effect on blood-pressure of the infusion of normal saline 
intravenously depends upon whether the pressure is normal or low 
at the time of the introduction. If the pressure be normal, Cohn- 
heim showed that large quantities of normal saline may be intro- 
duced intravenously with only very slight and transitory elevation 
of blood-pressure. This is because the fluid introduced is rapidly 
removed by the kidneys and intestines. When, however, the blood- 
pre sure is much below normal, either as the result of loss of vaso- 
motor tone or of hemorrhage, the effect of introduction of normal 
-aline is considerable and is persistent. The injection of defibrinated 
blood, however, as Mall has shown, always produces a marked rise 
of blood-pressure. It is possible by this means to raise and main- 
tain the aortic pressure very considerably above normal. This 
i- probably due to the content of colloidal substances in the blood 
which cannot be removed by kidney or intestine and which, being 
retained, retain the fluid also, knowlton- has shown that intra- 
venous injection of colloidal solutions, such as gelatin, causes a 
similar persisted rise of blood-pressure without diuresis. 

i M. Miller and E, M. Miller: Jour. Physiol., 1911, xliii. l'Il'. 
* Jour. Physiol., 191 1. \liii, 219. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 37 

That the lymphatic system to some extenl acts as a regulator of 
the amount of Mood is unquestionable. It-* action, however, is 
not very rapid and is limited in extent . It has Keen demon. t rated 
that a rise in arterial blood-pressure is associated with increa e in 
the proportion of erythrocytes, leukocytes, and di;. substance of 
the Mood, while a fall in arterial blood-pressure results in decrease 
in the proportion of these elements. This is probably largely to be 

explained by passage of the fluid elements of the lilood into the 

lymphatic channels or vice vi rsa a transfer which has been supposed 
to take place chiefly in the lungs. 
Viscosity of the Blood. Increase in the viscosity of the Mood 

inel-ea.es the ivsislance to its passage through the vessels and ill 

consequence tends to the elevation of blood-pressure, and vice versa. 
Clinically, thus far, no definite relationship has been established 
between the degree of hemic viscosity and the height of blood- 
pressure. 

Blood-pressure and Blood Flow. By the velocity of blood flow at 
any point is meant the rate at which the blood column is passing 
that point. In the aorta near the heart the velocity is great during 
the systole and almost zero during diastole. A- the .mallei- arteries 
are approached the velocity becomes less during systole and greater 
during diastole until in the capillaries and -mailer veins the velocity 
is constant throughout the cardiac cycle. The average 
decreases on passing from the heart to the capillaries since the total 
cross-section of the capillaries is far greater than the cross-section 
of the aorta. The average velocity increases on passing from the 
capillaries to the large veins as the total cross-section of the venous 
bed diminishes. The maximum velocity of flow in the larger arteries 
of the horse during systole has been found to be about 520 mm. 
per second. The average velocity of flow in the dog has been found 
to be about 250 mm. per second in the large arteries, about 60 
mm. per second in the femoral and renal veins, and about 150 nun. 
per second in the jugular vein. 

By volume flow of the blood is meant the amount of blood passing 
through an organ or vessel in a unit time. The volume flow per 
minute is called the minute volume. In studying the minute volume 
of blood flow in organs or parts of the body it is frequently desir- 
able to express the minute volume per 100 grams of substance. 
Obviously, the minute volume in the first part of the aorta equals 
the pulse volume (the output per cardiac beat) multiplied by the 
cardiac rate per minute, and is also the total volume flow for the 
entire body. 



38 PHYSIOLOGY OF BLOOD-PRESSURE 

The purpose of blood-pressure is the maintenance of blood flow. 
The volume flow between two points is determined solely by the 
difference of blood-pressure between these points and by the resist- 
ance to be overcome in the connecting vessels. An increased 
difference of blood-pressure between two points with the same 
resistance must result in an increased volume flow from the one to 
the other. Unaltered difference of blood-pressure between two 
points with diminished resistance will likewise result in an increased 
volume flow from the one to the other. Increase in the physiolog- 
ical activity of any organ of the body demands an increased volume 
flow through the organ. Practically all physiological changes in the 
resistance in the arterioles and capillaries, and in the arterial blood- 
pressure, are to be looked upon as the normal mechanism for secur- 
ing the proper distribution of blood to the various organs and tissues 
of the body. 

It is clear, however, that volume flow is not proportional to 
blood-pressure alone. Indeed, abnormally high blood-pressure may 
be associated with a diminished volume flow due to an abnormal 
degree of resistance in the peripheral vessels. This may be illus- 
trated by contrasting the effects (1) of abdominal pressure (which 
forces blood from the capillaries and veins of the abdominal viscera 
to the heart with an increase of the effective venous pressure at 
the heart, and an increased systolic output) with (2) the adminis- 
tration of adrenalin (which by constriction of the arterioles increases 
the peripheral resistance). Both procedures elevate the blood- 
pressure but they have opposite effects upon the pulse-pressure and 
upon the volume flow through certain vascular areas. 

Abdominal 
pressure. Adrenalin. 

Mi :ni aortic pressure I I 

Systolic aortic pressure I I 

Diastolic aortic pressure I I 

Aortic pulse-pressure I D 

Aortic volume flow I D 

Mesenteric volume flow I D 

Renal volume flow I D 

Brain volume flow I I 

I equals increased. 1) equals diminished. 



The following tables copied from Wiggers 1 gives an idea of the 
approximate volume flow through various parts of the body per 
LOO gm. of substance. 

1 Circulation in Health and Disease, Philadelphia and New York, 1915, p. 78. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 39 

Minute Volume peb LOO Grams Substance, 

Posterior extremity 5.0 c.c. Tschuewsky. 

Skeletal muscles 12.0 c.c. Tschuewsky. 

Heart 16.0 c.c. Bohr and Henriques. 

Head 20.0 c.c. Bohr and Henriquds. 

Stomach 21.0 c.c. Burton Opitz. 

Liver (arterial) 25.0 c.c. Burton Opitz. 

Portal organs (combined) . . . 30.6 c.c. Burton Opitz. 

Intestine 31.0 c.c. Burton Opitz. 

Spleen 58.0 c.c. Burton Opitz. 

Liver (venous) 59.0 c.c. Burton Opitz. 

Pancreas 80.0 c.c. Burton Opitz. 

Liver (total) 84.0 c.c. Burton Opitz. 

Brain 136.0 c.c. Jenson. 

Kidney 150.0 c.c. Burton Opitz. 

Thyroid 560.0 c.c. Tschuewsky. 

Systolic, Diastolic, and Mean Pressure. — In the discussion so far 
we have considered chiefly the effects of various factors upon mean 
blood-pressure and the relation of mean blood-pressure to blood 
flow. Inasmuch, however, as in clinical work it is not the mean 
pressure but the systolic and diastolic pressure that we measure, 
the relation of these to the mean pressure under various circum- 
stances must be considered. As already stated, there is no constant 
numerical relation between these three phases of blood-pressure that 
makes it possible from any two to calculate the third. It may be 
affirmed, however, that the mean pressure follows more closely in 
its fluctuations the diastolic pressure than it does the systolic, and 
the study of the diastolic pressure is therefore in many ways of 
greater value than is that of the systolic. Dawson's 1 rule for 
roughly estimating the mean pressure in man is to add one-third of 
the pulse-pressure to the diastolic pressure. Using an artificial 
circulation model, Wiggers has studied the effects of varying the 
peripheral resistance, the cardiac rate and the cardiac output upon 
the systolic, diastolic and pulse-pressure. The effects are tabulated 
by him as follows: 

Systolic Diastolic Pulse- 

pressure, pressure. pressure. 

Increased peripheral resistance . . . . + ++ — 

Decreased peripheral resistance ... — + 

Increased heart rate + + + — 

Decreased heart rate — + 

Increased systolic discharge ++ + + 

Decreased systolic discharge .... — — 

The systolic, diastolic and pulse-pressures are altered in the same 
direction by most procedures — not, however, always to the same 
extent. Under some circumstances, for example, in aortic regur- 

1 Loc. cit. 



in PHYSIOLOGY OF BLOOD-PRESSURE 

gitation, this is not the case, for the diastolic pressure is lowered 
while the systolic pressure is increased. In the average normal 
Individual al rest the diastolic pressure is 70 per cent, of the systolic 
pressure, but in not a few normal cases it may be as high as s ~> 
per cent. 

Pulse -pressure. — The pulse-pressure is with qualifications an 
indication of the cardiac output per beat. As a rule increased 
ventricular output leads to increased pulse-pressure and vic&jversa. 
The pulse-pressure normally ranges between 35 and 50 mm. Hg. 
With very few exceptions it should not fall below 20 per cent, of 
the diastolic pressure. The attempt has been made to establish 
formulas enabling one from the pulse-pressure and the cardiac rate 
to estimate alterations in the cardiac output per minute — in other 
words, of the blood flow from the heart. As a rule, changes in the 
pulse-pressure and in the aortic volume flow are in the same direc- 
tion; but this is not always true. For example, in aortic regurgita- 
tion, in which the pulse-pressure is extremely high, the volume 
flow through the aorta is usually approximately normal, being 
possibly a little higher or a little lower than normal, but not exhib- 
iting an increase in any sense proportional to that of the pulse- 
pressure. Arteriosclerosis also, increasing as it does the rigidity of 
the vessels, tends to produce a somewhat increased pulse-pressure 
with a somewhat diminished volume flow. Moreover, only under 
very limited conditions is there any constant quantitative relation 
between the respective changes in these factors. Hence all attempts 
aiming to express in figures the blood flow on the basis of the pulse- 
pressure should be regarded with suspicion. 

Effects of Respiration on Blood-pressure. — Ludwig, 1 in 1847, first 
showed that respiration affects the aortic pressure. The following 
analysis of these effects is from Tigerstedt. 2 

When the vagi are cut and the lungs are being artificially venti- 
lated, the capillaries of the lungs are compressed as the lungs are 
inflated, and dilated as the lungs are emptied. The first effect of 
inflation is therefore to drive the blood from the pulmonary capil- 
laries on into the left ventricle (.1) with increased output and rise 
of aortic pressure. The capillary constriction then acts as a dam to 
further transmission of blood, the inflow to the left ventricle dimin- 
ishes and aortic pressure falls (B). This is still more marked when 
the lungs are first deflated and the capacity of the pulmonary 
capillaries is increased (('). Once they become filled, however, 

\n ■!,. I. \n;ii. ii. Physiol., l n it, vi, 242. 
>Lehrbuch dea KreiBlaufes, 1893. 



BLOOD-PRI.ssi /,•/■: TllliUUGHOX T THE VASCULAR TRE1 U 

they readily transmit a liberal supply to the Left hearl and the 
aortic pressure rises ( /)), to be still further increased as inflation 
again begins (.1). II' respiratory movement be made \<r\ rapid, 
the phases />' and l> are eliminated and the highest pressure comes 
a1 i In- end of inspiration, the lowest at the end of expiration (Fig. 7). 
In natural respiration the relations are altered. I >nnn- inspira- 
tion the pulmonary capillaries are first distended and while filling 
with blood retard its onflow (A), but when dilated permit a ready 
Now through to the left hearl I B); with the beginning of expiration 



AORTIC 
BLOOD 

Phi ■ SURE 




inspiration expiration inspiration expiration 
Fig. 7 

they are compressed, emptied into the left heart with elevation of 
the aortic pressure (C), but during the remainder of expiration they 
offer considerable resistance to the onflow of the Mood (D) I Fig. 8). 

Erlanger and Festerling 1 find the phases .1 and C so long as to 
almost do away with phases B and J). They note toward the end 
of inspiration an acceleration of cardiac rate which tend- to increase 
aortic pressure, and toward the end of expiration a retarding of 
cardiac rate. 

These changes in cardiac rates, first noted by Ludwig, do not 
occur if the vagi have been cut; they are therefore reflex phenomena. 
Einhodt, Talma, Kronecker and Heinricius believe the aspiration 

AORTIC 
BLOOD 
PRESSURE l\ ^ 




of blood into the thorax during natural inspiration tends to increase 
diastolic filling, and diminish systolic emptying with a lowering of 
blood-pressure, and, vice versa, in expiration. Fredericq has shown 
that if in an animal with artificial respiration and cut vagi and 
phrenics the artificial respiration be suspended, respiratory move- 
ments of the thoracic wall occur. These are, of course, without 
effect either on the pulmonary blood flow or ventilation. However, 
during the inspiratory movement a fall of aortic pressure occurs; 

1 Jour. Exper. Med., 1912, xv, 370. 



42 PHYSIOLOGY OF BLOOD-PRESSURE 

during the expiratory movement, a rise. These changes can only 
be explained as effects arising from the vasomotor centre which 
induce alterations in peripheral resistance. There is therefore a 
coordination between the three centres, the respiratory, cardio- 
inhibitory, and vasomotor as follows: 

Respiratory. \ i^oranstrictor. Cardio-inb.ibitory. 

Inspiration Inhibition (dilatation) Cardiac acceleration 

Expiration Stimulation (constriction) Cardiac retardation 

Obviously the changes in the cardio-inhibitory and vasomotor 
centres have opposite effects on the blood-pressure. Fredericq's 1 
experiment shows that these changes are not due, as Schiff sup- 
posed, to changes in the gases of the blood, the result of pulmonary 
ventilation. 

The inspiratory fall of the diaphragm raises abdominal pressure, 
and serves as an adjunct to the aspirating action within the thorax 
in sending the blood from the abdomen into the thorax. 

Henderson has concluded from recent experimental studies that 
the variations in arterial pressure are of the same character and 
bear the same relations to the phases of respiration in an animal 
which is breathing spontaneously after the chest has been opened, 
as in a subject with the thorax intact. This would argue against 
the importance of the changes in intrathoracic pressure as an 
explanation of the respiratory changes in arterial pressure. He 
concludes that with normal venous pressure, the respiratory varia- 
tions of blood-pressure are always accompanied by and are due to 
associated changes in pulse rate, accelerated rate causing higher 
pressure. On the other hand, with a deficient venous pressure, such 
as exists frequently under experimental conditions, after hemor- 
rhage or in shock, forcible expiratory contractions of the diaphragm 
may increase the venous pressure sufficiently to more than compen- 
sate for a slower pulse rate during expiration. 

In animals under experimental conditions, the pulse as already 
noted, usually quickens during inspiration and slows during expira- 
tion. In man not only this relation but, according to Putzig, 2 the 
exact opposite and many intermediate synchronisms likewise occur. 
Henderson and Barringer find, however, that in the large major- 
ity of their studies both from man and animals, no matter what 
the relation of pulse rate to respiratory phase may be, arterial 
pressure rises with the cardiac acceleration and falls with retardation. 

1 Arch. Ital. dc Biologie, 1882, iii, 55. 

*Ztsehr. f. exper. Path. u. Therap., 1912, xi, 115. 



BLOOD PRESSURE THROUGHOUT THE VASCULAR TREE 43 

Summing up the typical effects of respiration on the cardio- 
vascular system under normal conditions we find: 

Inspiration: First, fall of aortic pressure; second, cardiac accel- 
eration, possibly slight rise of aortic pressure. 

Expiration: First, rise of aortic pressure; second, cardiac retarda- 
tion, possibly slight fall of aortic pressure. 

These fluctuations of pressure, synchronous with respiration, con- 
stitute the second order of blood-pressure oscillations. In norma] 
individuals these waves are a negligible factor in clinical observa- 
tions, but in labored respiration they may mount to 8 to LO mm. 

Pressure in the Pulmonary Circulation. Wiggers has recentlj 
reviewed the data upon this subject. lie found, using a maximum 
and minimum manometer, that the maxium pressure in a series of 
animals studied averaged 31.3 mm. Hg.; the minimum 5.9 mm. Hg., 
with a mean pressure of 19 nun. Hg. During apnea the maximum 
pressure falls and the minimum increases, so that less variation of 
pressure is observed in the pulmonary circulation during a period 
of apnea. Variations in the length of the cardiac cycle between 
0.6 second and 0.9 second, such as occur normally from beat to beat, 
are without influence upon the diastolic pressure in the pulmonary 
artery, and have only little influence upon the systolic pressure. 
Whenever, however, the output of the right heart increases, whether 
this be due to an increase in the venous pressure or to some influence 
modifying the contraction of the heart, the pressure is increased 
in the pulmonary artery and the flow augments. This increase in 
pressure and flow also extends to tbe pulmonary veins. The total 
pulmonary resistance is governed by the degree of lung expansion, 
the effect of negative pressure on the extrapulmonary vessels, vaso- 
motor variations, and altered vis a f route caused by impaired action 
of the left heart. Cloetta has shown that as the lungs enlarge a 
moderate distention diminishes the resistance, but an extreme 
distention augments it. 

Traube-Herring Waves. — These were first noted by Traube. 1 He 
observed that in a curarized animal with artificial respiration if 
the respiration was suspended, the aortic pressure rose and remained 
high for two or three minutes, and that during that time, without 
any movements of the animal or any respiratory movement, the 
arterial pressure showed slow waves, about seven per minute, that 
might have an amplitude of 40 mm. of mercury. The cardiac rate 
remained unaltered. After two or three minutes the arterial pressure 

1 Central f. d. med. Wissensch., 1865, iii, 881. 



44 PHYSIOLOGY OF BLOOD-PRESSVh'l- 

began to fall and from this moment these waves ceased, or at most 
a few feeble ones were observed. If, now, artificial respiration were 
resumed, these slow waves, perhaps only two per minute, might again 
for a while be observed, the waves due to the artificial respiration 
and to the cardiac cycles being superimposed upon them. He 
considered these waves the result of the stimulus of CO2 upon the 
vasoconstrictor centre, and succeeded in producing them by main- 
taining respiration with an atmosphere containing 20 per cent, of 
( '( k The tracing in Fig. 6 illustrates these oscillations. 

Intrapericardial Pressure. — If a cannula be introduced into the peri- 
cardium of an animal, the pericardium ligated around the cannula 
and normal saline introduced in such a way that its pressure may 
be measured and controlled, it. will be found that a very slight 
positive intrapericardial pressure will cause a fall of aortic blood- 
pressure with a diminished cardiac output. "When the pressure 
rises to even so low a figure as 8 to 10 mm. Hg. the cardiac output 
becomes practically nil and there is a rapid extreme fall of pressure 
due to occlusion of the great veins supplying the auricles, by an 
intrapericardial pressure exceeding the venous pressure. 

Intra-abdominal Pressure. — If, while recording the carotid or 
femoral pressure of a dog, pressure be exerted over the abdomen 
with the hand or in any other way, the arterial blood-pressure will 
be seen to rise 10 to 20 mm. Hg., and to remain at a somewhat 
elevated level while the pressure is maintained. This is due to 
the fact that, as already noted, the splanchnic vessels constitute 
the ureat reservoir for the blood. Increase of intra-abdominal 
pressure tends to empty' these vessels onward into the right auricle, 
and hence by increasing the venous supply to the heart to increase 
the cardiac output. At the same time the additional pressure 
increases somewhat the resistance offered to flow through the 
mesenteric capillaries, and hence resistance of the most important 
vascular area from the stand-point of the determination of blood- 
pressure. By both means increased intra-abdominal blood-pressure 
leads to increased arterial blood-pressure. Conversely, relaxation 
nf the abdominal walls favors low arterial blood-pressure with 
stasis of 1 Ik- blood in the splanchnic area, but this tendency may 
be entirely counter-balanced by adequate vasomotor tone in these 
vessels. 

Burton-Opitz 1 lias shown that an increased intra-abdominal 
pressure up to I'd \<> 30 mm. Hg. causes an increased blood How 

'The Carotid Blood Flow in Relation to ili<' Intra-abdominal Pressure, Am. 
Jour. Physiol., l'.Ul, xxxvi, 64. 



BLOOD PRESSl RE THROUGHOl T THE \ ASCI LAR TREE 15 

and blood-pressure in the carotid arteries and externa] jugular 
veins and also an increased blood-pressure in the femoral artery. 
There is e\ idently broughl about, therefore, a shifting of the blood 
from the splanchnic to the peripheral circulation and especially 

to the head under such conditions. 

Extremely high intra-abdominal pressure, as from a very large 
ascites, may interfere with the return of blood to the heart, and 
lower arterial blood-pressure. 

Hepatic Circulation.- Burton Opitz has studied the circulation 
through the liver and its vasomotor control. He finds that in a 
15-kilo dog the liver receives a How of Mood of aboul 120 c.c. per 
minute; therefore an amount of blood equal to the entire amount 
in the body traverses the liver every three minutes. Studies 
by means of the Strohmuhr showed that two-thirds of this blood 
is derived from the portal system and one-third from the hepatic 
artery. The portal pressure was about L0 nun. Hg. Stimulation 
of the splanchnic nerve led first to an increase of the portal How and 
a rise of the pressure in the portal vein soon followed by a diminished 
portal How and fall in the portal pressure. This, however, was 
compensated for by an increased How from the hepatic artery 
resulting from the increased aortic pressure that follows splanchnic 
stimulation. 

Blood-pressure and Intracranial Pressure. The brain is enclosed 
in a bony encasement and is, so to speak, floating in the cerebro- 
spinal fluid. This fluid fills the subarachnoid space, the ventricles 
and their communicating passages; all these spaces are normally 
in free communication. 

Evidence indicates that the pressure of the cerebrospinal fluid 
is always equal to the venous pressure in the brain sinuses. This 
pressure may vary from in the upright position (Hill) 1 to 50 to 
60 mm. Hg. in the convulsions of strychnine poisoning, or even 
more in cases of brain tumor. If the intracranial pressure exceeds 
the carotid pressure the circulation through the brain becomes 
entirely checked, due to compression of the capillaries. Complete 
occlusion of the larger cerebral arteries occurs, however, only when 
the intracranial pressure is raised (experimentally) to about 150 
mm. Hg. above the carotid pressure (Eyster, Burrows and Essick). 2 
The cerebral anemia produced by a rise of intracranial pressure 
to the level of the carotid pressure was shown by Cushing 3 to produce 

1 The Physiology and Pathology of the Cerebral Circulation, London, 1896; Proc. 
Royal Soc, 1894, lv, 52. 

2 Jour. Exper. Med., 1909, si, 489. 

3 Mitteil. aus den Grenz. der Med. u. Chir., 1902, is, 791; Am. Jour. Med. Sc, 
1903, exxv, 1017. 



46 PHYSIOLOGY OF BLOOD-PRESSURE 

two reflex effects: (1) stimulation of the vagus with slowing of 
the cardiac action; (2) stimulation of the vasomotor centre, with 
general vasoconstriction and rise of carotid pressure to the level 
of the intracranial pressure, and in consequence the reestablishment 
of the cerebral circulation. If the increase of intracranial pressure 
be very gradual the vagus excitation may not be elicited, dishing 
likewise studied the effects of localized pressure upon portions of 
the brain and obtained various results dependent upon the location 
selected. Pressure upon the medullary centres acts as does increase 
in general intracranial tension. The elevated blood-pressure asso- 
ciated with intracranial pressure secondary to neoplasms of the 
brain is to be considered a compensatory and beneficent process 
for the maintenance of blood flow through the vital centres. If this 
compensatory rise does not occur, absolute cerebral anemia results. 
The time that different portions of the brain can endure anemia 
and recover varies greatly. Experiments by Crile and Dolley 
showed that the central nervous system of young animals endures 
anemia better than that of older ones. Those parts of the brain 
which preside over conscious life, the higher psychic centres, were 
in no instances resuscitated after total anemia of eight minutes, 
but always after only four minutes. The vasomotor centre was 
frequently resuscitated after fifteen minutes, occasionally after 
eighteen, once after twenty, and once in a puppy after thirty 
minutes. The respiratory centre was more resistant, moderate 
reaction being obtained after as much as forty minutes of total 
anemia. We may say, therefore, that reduction of arterial pressure 
results in lessened blood supply and, as a rule, diminished activity 
within the brain; that if this reduction be great enough, complete 
anemia of the brain results with cessation of its activities, and 
unless the blood supply be promptly restored, a permanent cessa- 
tion ; also that the arterial blood-pressure, so far as it concerns the 
brain, must be considered with relation not to the atmospheric, 
but to the intracranial pressure, hence a rise of intracranial pressure 
is equivalent to a fall of blood-pressure, and vice versa. 

Blood-pressure and Intra-ocular Pressure.— The chambers of the 
eyeball an- filled with fluids which distend the eyeball and maintain 
a pressure in these cavities normally of about 20 to 30 mm. Ilg. in 
man. The intra-ocular pressure is measured by one of two methods : 
(1) Ophthalinouianometry, in which the pressure is measured 
directly by introducing a hollow needle into one of the chambers, 
preferably the anterior, and connecting it with a suitable manometer 
or system of manometers; (2) ophthalmotonometry, in which the 



BLOOD PRESSURE THROUGHOl T THE I iSCl LAR TREE 47 

degree of internal pressure is estimated by the amount of resistance 
to deformation offered by the walls of the eyeball. Obviously 

only the second method is, as a rule, applicable to man; it has, how- 
ever, certain fallacies and objections among which are the error 
introduced by the inherent rigidity <>l' the ocular walls, that due to 
the increase of intra-ocular pressure caused by the distortion of the 
eyeball, as well as the dangers and discomforts of the application of 
the instrument. These errors in the latest instruments are, however, 
largely eliminated. The pressures in the aqueous and vitreous 
chambers of the eye are practically identical, not differing by more 
than 1 mm. Hg. The distensibility of the walls of the eyeball is 
so slight that under ordinary conditions any increase in the fluids 
within the eyeball, either in one of the chambers or in vessels of 
the choroid, must cause an increase in the intra-ocular pressure. 
This fact leads to almost complete suppression of the visible pulsa- 
tion of the retinal arteries. Likewise the pressure in the blood- 
vessels, including capillaries and veins, can never fall below the 
intra-ocular pressure without collapse of these vessels and cessation 
of the flow through them. Since the outflow from the veins of 
the eye is usually a steady stream the venous pressure must be 
normally equal to the intra-ocular pressure. The capillary pressure 
within the eye is supposed by Parsons 1 to be 40 to 50 nun. Hg., 
and that in the veins to equal the intra-ocular pressure. 

The fluids distending the eyeball circulate along one of two 
courses: (1) That of the blood entering the ciliary arteries and 
leaving by the scleral veins, the venae vorticosse; (2) that of the 
lymph fluids filling the vitreous and aqueous chambers, entering 
the vitreous chamber from the vessels of the ciliary processes, passing 
into the aqueous chamber and leaving at the filtration angle by 
the spaces of Fontana for the canal of Schlemm and thence into 
the scleral veins. As long as the intra-ocular tension is to remain 
constant the combined inflow along these two courses must equal 
the combined outflow. All evidence indicates that the rate of 
secretion of lymph into the posterior chamber is proportional to 
intracapillary pressure in the eyeball. Therefore an increase of 
intracapillary pressure not only tends to increase intra-ocular 
tension directly, but also indirectly by increasing lymph production. 
Rapid changes in intra-ocular pressure are probably due, as a rule, 
to changes in intravascular pressure and volume; slower changes 
may be due to alterations in the rate of lymph formation or removal. 

1 Diseases of the Eye, Philadelphia, 1912. 



1- PHYSIOLOGY OF BLOOD-PRESSURE 

It is possible, as shown by ophthalmoscopic examination, to have 
distention of the retinal arteries and veins with normal intra- 
ocular tension due to compensatory adjustment in the quantity 
of lymph. As a rule, however, the intraocular pressure is closely 
related to the circulatory conditions in the eyeball. 

The Intro-ocular Pressure Rises- 1. With increase in the arterial 
pressure in the arteries supplying the eyes, as from compression of 
the thoracic aorta, stimulation of the vasomotor centre or of the 
splanchnic nerves, asphyxia, general effects of adrenalin, injection 
of normal saline, etc. At times the intra-ocular tension may be 
shown to vary with the respiratory or the Traube-Herring blood- 
pressure waves. 

L'. With local dilatation of the arterioles of the eyes. The exist- 
ence of vasomotor fibers for these vessels has not as yet been satis- 
factorily demonstrated, since changes in the intra-ocular pressure 
following stimulation or section of various nerves may in all cases 
be attributed either to effects upon the general blood-pressure, or 
to stimulation of the extra-ocular muscles (v. infra). 

3. From venous obstruction. Rise in general venous pressure 
is probably never sufficient to counter-balance the contrary effects 
of the associated fall of arterial pressure. Moreover, the relatively 
high venous pressure within the eyeball renders considerable changes 
in genera] venous pressure of but slight moment. On the other 
hand, local venous obstruction, as by ligation of the venae vorticosse, 
leads to marked rise of intra-ocular pressure (up to 90 mm. llg.), 
(Adamuk, Leber, Koster, Gzn) with increased transudation of 
highly albuminous lymph. There follows a slow return to normal 
pressure in the course of a few weeks. 

I. From increased lymph formation from any of the above- 
named causes of increased capillary pressure. 

.">. from decreased lymph drainage either from venous obstruc- 
tion or from obstruction of the filtration angle, as with pupillary 
dilatation in glaucoma. 

The intra-ocular tension fulls as the result of the reverse of the 
above-mentioned factors: 

I. From fall in blood-pressure in the arteries supplying the eyes. 

_'. From local arteriolar constriction such as may be obtained 
from adrenalin (Parsons) or nicotin (Henderson and Starling) 
by injection into the carotid, their local effects preceding their 
general systemic effects. 

'■'•. From diminished lymph formation secondary to any of the 
above-named causes ,,f reduced blood-pressure. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE I - 

4. From improved lymph drainage, as by freeing of the filtration 
angle by pupillary contraction. 

The Relation of Blood-pressure to Secretion. The activity of all 
glands is associated with increased blood flow through the -land. 
This increased blood How that is associated with glandular activity 
was early noted in connection with chorda tympani stimulation 
and the resultant abundant flow of saliva. It was naturally sug- 
gested that the abundanl flow of saliva might be entirely the result 
of the increased circulation and capillary blood-pressure in the 
gland, due to the vasodilator fibers in the chorda tympani. Ludwig 1 
showed, however, by measuring the pressure in the salivary duct 
by means of a manometer that following stimulation of the chorda 
tympani the pressure in the salivarj duct might exceed the blood- 
pressure. Moreover, if blood-pressure be shut off from the gland, 
stimulation of the chorda still gives secretion for a short time, 
whereas if atropin be injected into the gland, chorda stimulation 
causes dilatation of the vessels and increased blood flow but no 
secretion. Hydrochlorate of quinine injected into the gland causes 
vascular dilatation but no secretion. Therefore, while an abundant 
blood flow is essential for the proper functioning of actively secret- 
ing glands, it is not in itself the cause of the increased secretion. 

Effects of Exercise on Blood-pressure. — The effect of exercise on 
blood-pressure has been studied by many. One of the first inves- 
tigations was that of Marey 2 who measured the systolic pressure 
in the carotid of a horse before and after a run of ten minutes and 
noted a fall from 108 mm. Hg. before to 102 after. Kaufmann 3 
likewise found after prolonged exertion in horses a fall of pressure. 
Almost uniformly, however, the other observers, investigating for 
the most part the dog and man, have noted a rise in pressure after 
exercise. Tangl and Zunst 4 measured the maximal and minimal 
carotid pressures in the dog and from them calculated the approxi- 
mate mean pressure. After having the animal run up steps they 
found a rise of from 6 to 23 mm. Hg. After very severe exertion 
the elevation was extreme, amounting to 120 mm. Hg. Experiment- 
ing upon himself, von Basch 5 had, in 1887, noted after a quick ten- 
minute climb up a hill a rise from 125 mm. Hg. to 180 mm. Von 
Maximo wisch and Rieder 6 studied the effect on 27 individuals of 
2500 kg. of work performed on a Gartner ergostat in three to five 
minutes and they obtained in 21 individuals a rise; in 5 no change; 

1 L. Hill and W. Flack: Proc. Royal Soc, London, 1912, S. B., lxxxv, 312. 

2 Traveaux du Laboratoire, 1876. 3 Arch. f. d. ges. Physiol., 1892, liii. 

4 Ibid., 1898, lxx, 544. & Berl. klin. Wchnschr., 1887, xxiv, 206. 

6 Deutsch. Arch. f. klin. Med., 1890, xlvi. 
4 



50 PHYSIOLOGY OF BLOOD-PRESSURE 

and in 1 a fall of systolic pressure; the greatest rise was 50 mm. 
Hg.; the one fall was 20 nun. Oertel 1 in S individuals after moun- 
tain climbing noted a rise in all varying from 3 to 43 mm., the 
average being 17 mm. A rise after exertion has likewise been 
noted by Zadek, 2 Friedmann, Grebener 3 and Grunbaun, 4 Edge- 
comb and Bain, Eiehberg, 8 Russell, Williamson, 6 Routiner and 
Boussaguet, 7 and Graupner. 8 Moritz 9 obtained somewhat similar 
results. Brack 10 has noted in man with the Riva-Rocci and with 
the Hurthle apparatus an immediate rise upon commencing sudden 
severe exertion, up to 30 or 40 mm. Hg., followed after a few pulse 
beats by a fall to subnormal and then a prompt return to from 18 
to 38 mm. above normal. This brief primary rise he attributes 
to increased intrathoracic pressure. He measured the intrathoracic 
pressure by introducing a rubber bag into the esophagus and found 
it at the time of the primary rise of blood-pressure to be from 50 
to 130 mm. Hg. This pressure forces the thoracic blood on into 
the left ventricle and hence into the aorta with rise of pressure. 
The following brief fall he attributes to interference with the 
entrance of more blood into the thorax. 

Erlangef and Hooker, 11 making graphic records of maximal and 
minimal pressure in man, find that very moderate muscular exer- 
tion as, for example, walking, may diminish the minimal pressure 
while increasing the pulse pressure, pulse rate, and presumably the 
blood flow. More severe muscular exertion increases these and in 
addition the minimal pressure. 

Probably the chief cause of the increased pressure accompanying 
exercise is increased cardiac activity. A factor in influencing 
greatly the rise of pressure accompanying exertion is the degree 
of mental effort involved. An unusual form of exertion or one 
requiring close attention causes much more increase of pressure 
than the same amount of work performed in the course of habitual 
action. Thus, Karrenstein 12 found in 172 observations on 72 soldiers 
making a 5.7 km. march in seventy minutes, that 39.5 per cent. 
showed ;i rise, 10.3 per cent, no change, and 44.2 per cent, a fall; 
the average pressure before and after the march was unchanged. 

1 Therapied. kreislausfstorungen, v. Ziemssen's Handbuch d. allg. Therapie, vol. iv. 

Ztachr. f. klin. Med., L881, ii, 509. » Wien. med. Jahrb. , L882, p. L97. 

'• Wien. med, Presse, L899, \l. lit. 

\m. Med. Axn., kids, ]i. num. 
■ British Med. Jour., 1909, i, 530. 

pt. rend de 1m Soc. de biol., l>:nis, 1910, brviii, 1037. 
eh. med. W chnschr., L906, xxxii, L028. 
8 Deutsch. Arch. f. klin. Med., L903, Ixxvii, 339. 10 Ibid., 1907, xvi, .171. 

« .lnh,,s Hopkins Hospital Reports, 1904, xii, 53. 
B Ztschr. f. klin. Med., Berlin, L903, L, 322 (bibliography). 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TR1 

Of 39 observations on 25 soldiers following a two to three hours' 
march, L2.8 per cent, showed a rise and 69.2 per cent, a fall, the 

average being lowered from L06.1 to 98.8 i rig. In these cases 

little it' any mental effort was involved. The effed of mental 
effort has been shown by Putermann, 1 who studied with the Gartner 
tonometer the blood-pressure of t3 boys immediately before and 
after a school examination. A rise occurred immediately before 
the examination in 37, a fall in 1. The rise was usually LO to 20 
nun. Hg., but one rise of 50 nun. was noted. An\ excitement maj 
lend to ;i similar rise; indeed, the mere taking of the blood-pressure 
in a susceptible subject. This psychic rise affects the systolic 
pressure more than the diastolic The acceleration of the pulse 
during exercise is due to depression of the cardio-inhibitorj cenl re. 
It seems that the secondary fall of pressure due to peripheral vaso- 
dilatation is the result of depression of the vasoconstrictor centre 
and not of active vasodilatation, and that a similar depression of 
the respiratory centre may occur from cortical inhibition. 2 

Effects of Posture. — It has already been noted that the chief 
reservoir for the blood is the splanchnic area which of itself can 
contain all the blood of the body. Normally, an adequate return 
of blood from this reservoir to the right auricle is secured by means 
of the vasomotor tone of the splanchnic vessels. In the upright 
posture this return must occur against the force of gravity. In 
the recumbent posture, the antagonistic action of gravity is removed. 
Normally in man the reflex regulation of the splanchnic vasomotor 
tone is such that change from the recumbent to the upright posture 
is immediately compensated by an increased splanchnic vasomotor 
tone, and the aortic blood-pressure is maintained almost unaltered 
or there may be noted even a considerable rise of the diastolic 
pressure. In subjects with defective vasomotor compensation, how- 
ever, there may occur a fall of the aortic blood-pressure upon 
transition from the recumbent to the upright posture, and this may 
be of some diagnostic value. The common treatment of syncope 
by placing the patient recumbent has for its basis the effort to make 
gravity assist instead of resist the action of the splanchnic vaso- 
motor tone, which in this condition as in surgical shock and collapse, 
is inadequate. Change from sitting posture to standing causes, 
normally, according to most observers, a rise of from 5 to 15 mm. 
Hg. of systolic brachial pressure. Erlanger and Hooker, studying 

1 Wien. med. Wchnschr., 1904, liv, 265. 

2 Martin and Gruber: The Influence of Muscular Exercise on the Activity of Bulbar 
Centers, Am. Jour. Physiol., 1913, xxxii, 315. 



52 PHYSIOLOGY OF BLOOD-PRESSURE 

the minimal and pulse-pressures, found usually but not constantly 
on assuming the standing posture a rise in the minimal pressure, 
but a slight fall in pulse-pressure. Karrenstein 1 noted a little lower 
brachial systolic pressure in recumbent than in sitting posture. 
On stooping he found in 90.8 per cent, of 153 cases a rise of from 
1 to 45 mm. (average 10.8). The effect of posture upon vessels 
not at the level of the heart has been considered (p. 24). Baracb 
and Marks 2 upon changing the posture from the upright to the 
recumbent in an entirely passive manner in 48 subjects between 
fifteen and thirty years of age, have observed the following effects 
which differ from those of earlier observers: In changing from 
the erect to the horizontal the maximal pressure was usually 
increased, the cases varying from an increase of 28 mm. Hg. to a 
decrease of 20 mm. Hg. The minimal pressure was almost always 
diminished, varying from an increase of 4 mm. Hg. to a decrease 
of 44 mm. Hg. When the erect posture is resumed after five min- 
utes, the maximal pressure almost invariably falls and the minimal 
almost invariably rises. In the falling of the maximal pressure 
when the erect posture is resumed, it will nearly always fall con- 
siderably below the previous height of the first reading, while the 
minimal pressure may be higher or lower than the first reading 
with almost equal frequency. The pulse-pressure in its variations 
follows closely the maximal pressure. Persons with poor muscular 
development show a tendency to reversal of the pressure curve. 

Effect of Feeding. — After eating a full meal Karrenstein 3 noted 
usually a rise of systolic pressure of 10 to 20 mm. Erlanger and 
Hooker 4 obtained variable effects upon minimal pressure, but a 
constant increase of pulse-pressure. These authors noted a slow 
increase of pulse-pressure throughout the day, it being smallest 
in the early morning before rising. They found immersion of the 
body in warm water to increase minimal pressure, pulse-pressure 
and pulse rate; in cold water to increase minimal pressure, but to 
decrease pulse-pressure and rate. Immediately after the ingestion 
of food the systolic pressure rises (about 8 mm. Hg. in healthy 
young adults), then gradually falls until the beginning of the next 
meal. The diastolic pressure is much less and variably affected 
by feeding. Associated we find an increased pulse rate and pulse- 
pressure. 5 

»Loc. cit. \p-li. Int. Med., 1913, xi. Ivv 

» Loc. cit. * hoc cit. 

8 Weysse, H. W., and Brenton, It. I>.: Diurnal Variations in Arterial Blood- 
pi • --urc, Am. Jour. Physiol., 1915, xxxvii, 330. 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 53 

Sleep. — Tarchanoff 1 noted a fall of aortic pressure in young 

dogsof 20to50] Hg. during the early stages , of sleep. Leonard 

Hill,- Brush and Fayerweather, 3 Howell and Brooks, and Carroll 4 
have studied the phenomenon in man and note the greatest fall 
one or two hours after commencement of sleep; this may amount 
to 20 mm. Then begins a gradual rise continuing to the maximum, 
usually reached about 5 P.M. the following day. If sleep is dis- 
turbed the usual drop is less profound. In day sleepers it is the day 
pressure which is lower than the night. The minimal blood-pressure 
is according to Weysse and Lutz very uniform throughout the day, 
but with a tendency to a slight lowering as the day progresses. 

Altitude. — The study of the effects of altitude on blood-pressure 
has been approached in two ways: 1 1 ) By the study of the blood- 
pressure of individuals remaining for longer or shorter periods at 
various altitudes, and (2) by the use of the pneumatic chamber to 
change the atmospheric pressure. 

The blood-pressure may either be measured as so many milli- 
meters of mercury above the surrounding atmospheric pressure, 
or the absolute pressure of the blood may be measured. It ma; be 
stated at once that changes in atmospheric pressure are associated 
with approximately equal changes of the absolute blood-pressure 
in the same direction. Thus, if at 760 nun. atmospheric pressure 
(ordinary atmospheric pressure at sea level) the absolute systolic 
blood-pressure is 895 mm. (135 mm. above atmospheric pressure), 
then if the atmospheric pressure be reduced to 460 mm. the absolute 
systolic pressure will be reduced to about 595 mm. Since all the 
manometers ordinarily used measure the elevation of the blood- 
pressure above the surrounding atmospheric pressure, it is this 
difference of pressure that is ordinarily discussed. Moreover, it is 
this difference of pressure and not the absolute pressure which is 
the measure of the functional activities of the circulatory system. 
It is to be understood, therefore, that whenever pressure is here 
referred to it is the pressure in excess of the surrounding atmospheric 
pressure, that is, the relative blood-pressure, that is meant. 

The first to study the effects of changes of atmospheric pressure 
upon the blood-pressure was Paul Bert. 5 Upon lowering the 
atmospheric pressure he obtained a slight diminution of the relative 
blood-pressure. 

1 Arch. Ital. de Biol., 1894, xxi, 318. 

2 Lancet, 1898, i, 282. 3 Am. Jour. Physiol., 1901, v, 199. 

4 Tr. Assn. Am. Phys., Philadelphia, 1912, xxvii, 8. 

5 La Pressure barometrique, Paris, 1878. 



54 PHYSIOLOGY OF BLOOD-PRESSURE 

Lazarus and Schirmunski' in 1884 studied a man in the pneumatic 
chamber with the following results: 



Atmospheric pressure. 


Relati 


\ e sj stolic blood-pressure. 


mm. 1 1 g 




mm. Hg. 


760 




135 


670 




L35 


440 




1321 Subjective 


380 




110/ dyspnea. 


460 




118 


660 




1 35 


760 




130 



( !amus 2 with rabbits in a pneumatic chamber reduced the pressure 
from 760 to 200 mm. with, in some animals, little or no fall of the 

relative Mood-pressure, but with other rabbits on reaching about 
250 mm. atmospheric pressure the relative blood-pressure showed a 
marked fall. 

Mosso, 3 with a dog in a pneumatic cabinet, with reduction of 
atmospheric pressure to 228 mm. Hg., obtained a slight fall of 
relative blood-pressure. On the other hand, Frankel and Geppert 4 
and also Dietrick with lowered atmospheric pressure obtained a 
slight rise of relative blood-pressure, while G. Liebig 5 obtained a 
rise in 2 men, but in 2 others a fall. 

The approximate relation of atmospheric pressure to altitude 
is shown in the following table from Camus: 8 

Atmospheric pressure, Altitude, Altitude, 

mm. Eg. meters. feet. 

760 

660 1,148 3,760 

560 2,370 7,700 

160 4,022 13,200 

360 5,945 L9.470 

260 8,600 28,180 

200 11,000 36,040 

Studies of individuals actually at various altitudes are not 
numerous. 

Schneider and Hedblom 7 studied the effect on a series of individ- 
uals passing from L700 elevation to 6000 feet and again later from 
6000to 1 l,109feet. In passingfrom 1700 to 6000 feet they observed 
falls of relative pressure of from 3 to 7 mm. Hg., with no changes 

Ztscbr. f. klio. Med. L884, vii, 299. 
- Jour, de phj Biol, et de pal bol. gen., Paris, 1903, v, 6 13. 

Vrch. [tal. de Biol., L909, xliii. 
4 Ueber die Wirkungen der verdiinnte Lull, Berlin, 1883, p. 65. 

iingsberichte d. gesellsch. f. Morphol. u. Physiol., Munich, 1896, rii, 37. 
' Loc. 'ii . 
7 Am. .lour. Physiol., L908 9, xxiii, 90 (bibliography), 



BLOOD-PRESSURE THROUGHOUT THE VASCULAR TREE 55 

in the average diastolic pressure. In passing from 6000 to I t,109 
feet they found an average fall of both systolic and diastolic pressures 
of 7 mm. Hi;., and an average rise of pulse rate of 26 beal per 
minute. The effed upon the systolic pressure was more constant 
than that upon the diastolic. The effect of the altered altitude was 
most marked immediately following the arrival at the nev 
and those individuals showed mosl changes who were mosl affected 
subjectively by the change of altitude. Small changes of elevation 
were without any effect. 

Staehelin 1 studied blood-pressure during balloon ascensions to 
a height with atmospheric pressure of 690 nun. without noting 
any effect on either systolic or diastolic pressure. Staubli 2 noted 
at St. Moritz (5800 feet) no constant change in the blood-pressure 
of healthy subjects. 

( lough 3 has recently published studies of the effects of a rapid 
descent of 1700 feet in a mine shaft. lie found that the rapid change 
in altitude either up or down frequently caused a fall of systolic 
pressure of 5 mm. He detected no significant difference between 
the average blood-pressure of individuals living at the altitude of 
5000 feet and those at sea level. 

Gardiner and Hoagland 4 studied individuals living for a year 
at an altitude of 6000 feet and found their relative pressure- only 
slightly lower than those observed in individuals of the same age 
at sea level. They studied the systolic pressures of 22 college hum 
going by train from a level of 0000 feet to 1.4,109. The average 
relative pressure at GOOO feet was L26 nun. Ilg.; on arrival at 14,100 
feet, 121 mm. Hg.; three and a half hours after arrival, 118 mm. 1 [g. 
Smith 5 in a recent study has concluded that an altitude of 6230 
feet does not produce any consistent alteration of blood-pressure 
in either normal or tuberculous individuals. 

Schneider, Cheley, and Siseo 6 have studied the effect of physical 
exertion upon the blood-pressure at very high altitudes (14,900 feet). 
^Yhile the arterial blood-pressure at rest was found to be unchanged 
or a trifle lower at this high altitude, the effect of exertion was to 
induce a much more marked rise of pressure than would follow r the 
same degree of exertion at lower altitudes or at sea level. This 
increased reaction to exercise was most conspicuous during the first 
days of residence in the high altitude, was slightly lessened by 

1 Med. Klin., 1909, v, 361. 

2 Verhandl. d. Kong. f. inn. Med., 1910, p. 695. 

3 Arch. Int. Med., 1913, xi, 590. 4 Tr. Am. Climat. Assn., 1905. 

5 Effect of Altitude on Blood-pressure, Jour. Am. Med. Assn., 1915, hdv, 1812. 

6 Am. Jour. Physiol., 1916, xl, 380. 



56 PHYSIOLOGY OF BLOOD-PRESSURE 

acclimatization and did not wholly disappear after a residence of 
two weeks. The average rise in systolic pressure after a quick, 
short run was in three normal individuals 61 mm. Ilg. During 
exertion, arterial pressure rose more rapidly at high altitudes than 
at low altitudes; but whereas at low altitudes the arterial pressure 
reaches its maximum, after exertion, before the pulse rate, at the 
high altitude, the pulse rate reaches its maximum before the blood- 
pressure. 

Age.— In children the blood-pressure has been declared by 
Michael 1 to be more closely proportional to the height or weight 
than to the age of the child. Sex during childhood appears to be 
of no importance. 

Systolic pressure (Michael), 
Weight. mm. Hg. 

Infancy 75 to 90 

30 to 40 pounds 95 

40 to 50 " 100 

50 to 60 " 107 

60 to 70 " 112 

70 to 80 " 116 

80 to 90 " 122 

90 to 100 " 126 

Judson and Nicholson 2 give the following table of averages at 
different ages based upon a series of 2300 observations made with 
a modified Erlanger method and by the auscultatory method 
reading the diastolic pressure at the beginning of the fourth phase. 

Age. Systolic. Diastolic. 

3 years 91.8 65.6 

4 " 91.6 64.9 

5 " 91.3 64.4 

6 " 92.6 67.3 

7 " 94.0 66.3 

8 " 93.6 64.7 

9 " 94.3 71.0 

10 " 99.2 67.1 

11 " 97.1 65.5 

12 " 102.3 65.2 

13 " 103.6 70.5 

14 " 106.1 67.4 

15 " 105.6 67.5 

During adult life the normal systolic blood-pressure may be 
inferred from the following table from Woley. 3 

Systolic blood-pressure. 
\:'< High. Low. Average. 

15 to 30 years 141 103 122 

30 to 40 " 143 107 127 

40 to 50 " 146 113 130 

•".<M„60 " 149 115 132 

00 to 65 " 153 120 138 

1 k. Study of Blood-pressure in Normal Children, Am. .lour. Die. Child., 1911, i, 272. 
> Am. Jour, Dis. Child., L914, viii, 257. 3 Jour. Am. Med. Assn., 1910, lv, 121. 



EFFECTS OF ALTERATION OF BLOOD-PRESSURE 57 

Women during adult life average, according to Woley, about 

8 imii. lower in systolic pressure than males of the same age. The 
diastolic pressure is normally, at rest, about 70 per cent, uf the 
systolic. (See p. 134.) 

The average minimal pressure in healthy young males of twenty 
years of age was found by Weysse and Lutz to be 85 mm. I [g., with 
a maxima] pressure of 120 mm. 

Melvin and Murray, 1 in a series of normal cases using the aus- 
cultatory method and reading the diastolic pressure at the begin- 
ning of the fourth phase, find the normal diastolic pressure to 
range from 50 to 82 with an average value of 66, or 56 per cent. 
of the systolic. This is much lower, however, than the generally 
accepted figure. 

THE EFFECTS OF ALTERATION OF BLOOD PRESSURE 
UPON THE ORGANS OF THE BODY. 

I. Effects upon the Heart.— The first effect of a sudden elevation 
of aortic pressure through increase of peripheral resistance is, as 
we have seen (see p. 33), a reflex inhibition of the heart tending 
to reduce the cardiac output and restore the blood-pressure to 
normal. When a permanent increase in the peripheral resistance 
develops, be it the result of continued arteriolar spasm or of arterio- 
lar fibrosis, although the cardiac output per minute may be, and 
probably often is, diminished, the force of the ventricular systole 
is increased to meet the higher aortic pressure and deliver its output 
against this, and if the nutrition of the heart be good there develops 
a cardiac hypertrophy chiefly of the left ventricle. It may readily 
be seen that this phenomenon is a necessary compensatory adjust- 
ment if an adequate blood flow through the more resistant arterioles 
is to be maintained. It has been further suggested that the hypo- 
thetical substances which, circulating in the blood, have called 
forth the arteriolar spasm may also act as a direct stimulant to 
the cardiac muscle. This, for example, is true of adrenalin. In 
favor of this view 7 is the fact that hypertrophy in hypertension 
cases in man can be observed, as a rule, not only in the left ventricle 
but in all four chambers of the heart; the hypertrophy of the left 
ventricle is usually greater, however, than that of the other cham- 
bers (Senator). 2 It has also been suggested, but less favorably 
received, that the cardiac stimulation is the primary effect of these 

1 British Med. Jour., 1914, ii, 500. 

2 Die Erkrankungen der Nieren, Wien, 1902, p. 114. 



58 PHYSIOLOGY OF BLOOD-PRESSURE 

hypertensive substances, the arteriolar spasm and fibrosis being 
secondary. Experimental evidence bearing upon this point is 
difficult to obtain and to interpret, and the question remains 
unsettled. 

The final effect upon the heart of maintaining for a prolonged 
period a blood-pressure considerably above normal is cardiac 
exhaustion beginning, as a rule, with dilatation and weakening of 
tin- left ventricle. Then follow with falling blood-pressure, which 
may still, however, be considerably above the normal, the signs of 
circulatory failure throughout the body: edema, accumulation of 
fluid in the serous cavities, venous congestion, cyanosis, dyspnea, 
edema of the lungs, renal insufficiency, and the disturbances of 
the internal organs resulting from passive congestion. This out- 
come is hastened by coronary sclerosis, which impairs the cardiac 
nutrition. The effect of low blood-pressure upon the heart is, as 
a rule, to call forth a reflex acceleration of cardiac rate and activ- 
ity. So far as the coronary circulation suffers from the lowered 
blood-pressure a detrimental influence is exerted on the cardiac 
nutrition. 

n. Upon Arteries and Arterioles. — Associated with continued high 
blood-pressure are, in the great majority of cases, certain changes 
in the vessel walls. These consist of fibrous thickening of the inner 
and outer coats of the arteries and arterioles with increase of their 
elastic tissue. The muscular coat shows sometimes a thinning, 
sometimes a thickening, but the latter is due more often to increase 
of the fibrous tissue of the muscular coat than of the muscle tissue 
itself. Thai these fibrous changes in the vessel walls are the direct 
resull of strains or minute tears consequent upon the high blood- 
pressure has been suggested. That they are the direct effect of 
those toxic substances which have produced the arteriolar spasm 
and high blood-pressure is possible. Finally, in some cases these 
arteriosclerotic changes in the vessel walls result from the toxins 
of acute infections or of syphilis and develop before any rise of blood- 
pressure has occurred; once developed, however, they increase the 
resistance to the flow of blood through these vessels. The effect 
of this in leading in turn to a rise of arterial blood-pressure and 
eventually, if the COronaries be not too sclerosed, to cardiac hyper- 
trophy, will be discussed later. 

HI. Upon Capillary Pressure, Venous Pressure, and the Pulmonary 
Pressure. On these high arterial pressure has little effect. The 
arterial pressure is confined between the left ventricle on the one 
hand and the "stopcock," the arterioles, on the other hand, and 



EFFECTS OF ALTERATION* OF BLOOD PRESSURE 59 

marked changes maj occur in the arteria] pressure with no change 
whatever in the pressure in the capillaries, veins, or pulmonarj 
vessels. 

As we have noted, the capillary pressure is dependeni more upon 
the venous than upon the arterial pressure. 

IV. Upon the Kidneys. Goll's experiments, performed under 
Ludwig, were the 6rs1 to show conclusively the effect of changes in 
blood-pressure upon the activity of the kidneys. Goll cu1 the vagi 
of a dog, determined the blood-pressure by means of a cannula 
introduced into the carotid, then from the two ureters collected all 
the urine excreted for half an hour. He then stimulated continu- 
ously with a weak faradic currenl the peripheral end of one of the 
cut vagi, thereby diminishing the cardiac activity and causing a 
fall of blood-pressure. This procedure was continued for halt' an 
hour, during which time the urine from the ureters was again col- 
lected. It was found that the fall in blood-pressure had markedly 
reduced the amount of urine excreted in the half-hour and thai it 
had reduced the water of the urine more than it had the solids, so 
that while the actual amount of solids was reduced, the percentage 
of solids and the specific gravity of the urine were increased. 

He then took another dog and similarly recorded the carotid 
pressure and measured the urine excreted From the two ureters lor 
half an hour. lie then Med the dog freely; a fall in blood-pressure 
resulted and persisted. During the next half-hour, while the 
blood-pressure was low, the urine was again collected and was found 
as in the first experiment to he reduced in amount; again the water 
w r as more reduced than the solids. The blood which had been 
withdrawn from the animal was defibrinated and at the end of 
the half-hour was reinjected, restoring the animal's blood-pressure 
to about the original level. The urine was now again collected for 
half an hour and was found to have increased in quantity to about 
the original level of excretion and the water had increased more 
than the solids, so that while the elimination of solids had increased, 
the percentage of solids and the specific gravity were reduced to 
about normal. 

Later Meyer performed the following experiment: In a rabbit 
he constricted the vena cava above the entrance of the renal veins 
to half its natural diameter. This, he found, led to the excretion 
of a diminished quantity of highly concentrated urine which con- 
tained albumin. 

It will be observed that, although Meyer's experiment increases 
the blood-pressure in the capillaries of the kidney, it diminishes 



60 PHYSIOLOGY OF BLOOD-PRESSURE 

the output of urine. The activity of the kidney is not, therefore, 
proportional to the blood-pressure, as Coil's experiment might sug- 
gest, but to the rate of blood flow through the renal vessels. In 
both of Coil's experiments the fall of blood-pressure reduces the 
flow through the renal vessels, and in Goll's second experiment the 
reinject ion of the blood with the resultant rise of pressure increases 
the flow through the kidney. In the same way digitalis, which 
increases the amplitude of the cardiac systole and thus augments 
the cardiac output, thereby raising the blood-pressure and thus 
increasing the blood flow through the organs, is a drug which pro- 
duces diuresis. On the other hand, adrenalin, when injected intra- 
venously, increases the arterial blood-pressure much more than does 
digitalis, but does so by constriction of the arterioles and therefore 
reduces the blood flow through the organs. The effect of a large 
dose of adrenalin upon the excretion of urine is to greatly dimin- 
ish or entirely stop it during the brief period of the drug's effective- 
ness. The comparison of the effects of these two drugs on renal 
activity is a good illustration of the impossibility of estimating the 
effectiveness of the circulation by the arterial blood-pressure. 

Nitroglycerin and the nitrites act chiefly by dilating the arterioles 
and thus lowering blood-pressure. Did they influence all arterioles 
equally their effect would be to increase the blood flow through all 
the organs, with a lowering of blood-pressure. In fact, however, 
they dilate the mesenteric vessels disproportionately. Very small 
doses may lead to increased blood flow through the kidneys with 
diuresis. However, larger doses dilate the mesenteric arterioles 
so much more than the renal that the blood flow is diverted through 
the former with a fall of aortic pressure, and the flow through the 
renal vessels diminishes, as does the urinary output. 

We find, therefore : (1) A rise in the general arterial blood-pressure 
caused by increasing the bulk of the blood or by augmenting the 
cardiac output, increases the blood flow through the kidneys and 
in consequence the renal activity. (2) A change in the general 
arterial blood-pressure (rise or fall), produced in such a way as to 
diminish the blood flow through the kidneys, diminishes the renal 
activity. 



CHAPTER II. 

THE INSTRUMENTAL ESTIMATION OF 
BLOOD-PRESSURE. 

No one who has had any experience with instruments of precision 
in controlling his tactile impressions, will flatter himself with the 
delusion that he can gauge endovascular tension with anything 
approaching accuracy with the finger. Extremes are easily recog- 
nized but the intervening moiety is a fertile source of error. The 
size of the vessel, the character of the surrounding tissues, the 
volume of the pulse and the state of the arterial wall itself, all 
contribute to one's confusion. The estimate of arterial tension has 
therefore been relegated to the more exad field of sphygmoman- 
ometer measurement, just as has the determination of alterations 
of bodily temperature to the thermometer. 

With the older methods ami with must of the early instruments 
only the systolic pressure could be gauged. This is no longer suffi- 
cient. It is now possible to estimate the diastolic pressure with 
approximate accuracy by a number of different methods. The 
systolic index alone tells but a part, and that but a small part, of 
the whole story. No examination can be considered satisfactory 
or complete which does not include the diastolic pressure. Indeed, 
the latter is often more important than the systolic reading. 

A large number of instruments for the estimation of human 
blood-pressure have been devised and modified. This gradual 
development will not concern us here, as the subject is mainly his- 
toric in its interest and has already been ably described by others. 1 
In many of the older instruments, either the principle was faulty or 
the technic unsatisfactory, hence we shall consider mainly those 
which are of practical utility today. 

Nearly all of the modern instruments are constructed with an 
elastic cuff or arm band which, when inflated and encircling one 
of the extremities, compresses, and when the pressure is raised 
sufficiently, obliterates the arterial pulse below the cuff. This 

1 Janeway: The Clinical Study of Blood-pressure, New York, 1904, p. 43. Tiger- 
stedt: Lehrbuch d. Physiologie d. Kreislaufes, Leipsic, 1893, p. 321. Ergebniss der 
Physiologie, 1907, vi, 265. Vacbide and Lahy: Arch. gen. de med., 1902, pp. 339, 



62 INSTRUMENTAL ESTIMATION OF BLOOD PRESSURE 

point corresponds to the systolic pressure. It indicates the point 
at which the external pressure is just sufficient to overcome the 
internal resistance (blood-pressure, velocity, the arterial wall, and 
the surrounding soft tissues). The velocity factor is negligible and 
the resistance of the arterial wall and soft tissues normally does 
not exceed 10 to 7 mm. respectively. Hill has shown that the 
obliteratioD pressure in the femoral artery of the dog is the same 
(within 1 to 2 nun. Hg.) as the systolic pressure taken in the opposite 
femoral with a cannula and the Iliirthle manometer. 

The amount of pressure required is measured by means of 
either (1) a mercury manometer graded in millimeters; (2) an 
aneroid; (3) a metallic spring manometer; or (4) a compressed-air 
manometer with an indicator; depending upon the particular 
instrument employed. 




lie '.». —Arm in cross-section with Riva-Rocci cuff: R, outer wall of rubber tube; 
A", inner wall of rubber tube; S, screw fastening ; D, clamp; C, silk cover; .1, brachial 
artery; //, humerus; T, tube leading to manometer'. 

The Character of the Cuff. — The compression may be exerted upon 
the vessel in question either by (a) a limb-encircling, distensible 
elastic cuff (applied to a segment of the arm or leg), or (I>) by means 
of a solid or a fluid pad overlying the artery; in either case sur- 
rounded by an external inexpansile fabric. Of these the former is 
mi ii-c satisfactory (see Fig. 9). 

The accompanying figures illustrate the principles involved in the 
application of a cull' to the arm. In Fig. '.» we have a rubber cuff 
completely encircling the arm, but insufficiently inflated to occlude 
the artery. In Fig. 10 the rubber extends only part way around 
the arm, but the pressure is high and the arterial lumen therefore 
Completely obliterated. 

The width of the cuff, as was shown by von Recklinghausen, 1 is 

1 CJeber Blutdruckmessung beim Menschen, Arch. f. exper. Path. u. Pharmakol., 
1901, dvi, 78. 



THE CHARACTER OF THE CUFF 



63 



of vital importance. If it is too narrow, readings higher than the 
actual endarterial pressure maj be obtained. The soft tissues of 
the arm offer considerable resistance to compression, which may, 




^^ 



Fig. I". — Ann in cross-sectioD with Hill and Barnard cuff: R, outer w:tll of rubber 
Ikik; A", inner wall of rubber l>:ii_ r ; S, strap, fastened by buckle; C, leather cuff; 
-I, brachial artery; //, humerus; T, tube leading to manometer. 

however, be largely overcome l>\ lengthening the segment included 
in the cuff. The reason for this is shown in Fig. 1 1. 

If a distended artery is partially obliterated by the pressure of 
a single block — as in the case of a narrow cull' we not only have 



■■■■■■ 





W W 

Fig. 11 



to overcome the internal pressure of the vessel but also the oblique 
tension of the wall and surrounding tissues (W-T), and as a result 
too high readings are obtained. With a series of blocks exerting 



64 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

a similar pressure to the square inch, only the outer blocks (IV) 
will be concerned in overcoming the pull of the artery and tissues 
at U'-T. while the intervening ones (S-S) will exert their full 
pressure. 

With a Broad cuff an error of +7 to +9 per cent, may be assumed. 
With a narrow cuff the figure may reach +40 per cent., while 
the Gartner finger ring has a margin of error of +19 per cent. 

Blood-pressure instruments based upon obliteration of the pulse 
by pressure between a bone and a rubber bag (temporal, dorsalis 
pedis, etc.) deform the artery and shut off the blood flow below 
the systolic pressure. As has been pointed out by Hill and 
McQueen, 1 compression of the tissues surrounding the artery, so 
as to block the venous outlets, is essential to accuracy. This con- 
gests the blood beneath and beyond the armlet or bag. The pul- 
sating of the congested mass of tissues renders armlet or bag cap- 
able of delivering a circular compression to the artery and prevents 
deformation of the artery until the systolic pressure is exceeded. 

There was for a time much discussion as to the accuracy of von 
Recklinghausen's contention, caused by the belief that a cuff of 
12 cm. interfered with the progression of the pulse wave and yielded 
subnormal values. But the correctness of his view has now been 
definitely established by experiments (1) on the cadaver with arti- 
ficial circulation (Gumprecht); (2) on animals (Fellner, Rudinger, 
Schelling and others) ; (3) on the living human subject (0. Miiller 
and Blauel, Janeway). A narrower cuff may be advantageously 
employed for children (3 inches, 7 cm.). 

The outer covering of the elastic cuff, whether of canvas, leather, 
or cloth, must be of a non-distensible character and the rubber 
tubing connected therewith must be sufficiently inelastic to prevent 
any oscillation or stretching with increased pressure. If these 
facts are overlooked we introduce a new source of error for which 
we should have to allow with each increment of pressure. For this 
reason the outer covering must completely enclose the elastic cuff, 
which must not be allowed to slip out of place while in use. With 
a view of obviating this possibility, some cuffs are constructed in 
which the outer and inner cuffs are made as one piece (Vaquez, 
Uskoff, Oliver, Janeway). 

The elastic cuff must of course be sufficiently thin and flexible 
to add but a negligible increment to the manometrical pressure. 
This desideratum, as shown by Gumprecht, is easily furnished. 

1 Theory of Blood-preasure Measurement, British Med. Jour., June 24, 1916, 

X-. L'S95. 



PALPATORY METHOD 65 

The Location of the Cuff, etc. The brachial artery is usually 

selected for Mood-pressure estimation because of its accessibility, 
and because either in the erect, sitting, or recumbenl postures ii is 
at about the cardiac level. The presence of a thin shirt or waisl 
between the arm and the cull' produces only a negligible error. In 
fact it is much better to have a shirt interposed hut evenly dis- 
tributed than to have a tight sleeve or an undershirl rolled up 
into an arm-encircling band above the cuff. Thick sleeve- may 
yield readings from 10 to 20 nun. higher than the actual pressure. 
In children the thigh is often the preferable site, on account of the 
smallness of the arm. In adults, especially for purposes of compara- 
tive study, either the thigh or the calf may he chosen. The brachial 
artery is considered the site of choice because "it gives us the 
systolic lateral pressure within the subclavian, since brachial and 
axillary are continuous in direction, and therefore a near approxi- 
mation to systolic lateral pressure in the aorta. This combined 
with estimation of diastolic lateral pressure in the brachial, which 
is practically the same as aortic diastolic pressure, gives the best 
insight into actual variations of systemic blood-pressure" I Janeway ) . 
This statement has been questioned by some observers since as 
was first shown by Bing, the pressure in the two brachial arteries 
of the same individual may vary 20 mm. or more. The brachial 
pressure is generally, hut by no means invariably, canal to that uf I la- 
aorta. 

The cuffs furnished with the Tech and the Mercer instruments 
are so constructed that the stethoscope used for the auscultatory 
method is applied at the level of the cuff and not below it, as is 
usually the case. This gives readings on the average 10 mm. 
higher than those obtained in the usual manner and, in the opinion 
of the author, adds an unnecessary increment of error. 

I. PALPATORY METHOD. 

A. Estimation of the Systolic Pressure. — Method of Application for 
Instruments of the Riva-Rocci Type (Fig. 12). — The rubber cuff 
( D) (which should be 12 cm. in width) is applied so as to encircle 
the arm or leg, secured by a non-distensible canvas or leather 
cuff, and strapped or tied snugly in place (generally above the 
elbow or knee). The tube connecting with the rubber cuff is 
attached to the manometer (M) (the valve C On the latter being 
opened to admit air), and is inflated by means of a syringe 
bulb or pump (P) from the distal side of the manometer. The 
5 



00 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

systolic pressure is read by placing the finger on the radial pulse 
and pumping the mercury well above the point at which the pulse 
at the wrist disappears. We then close the valve C, open the 
second escapement valve E, and as the mercury falls note the 
point at which the radial pulse again becomes perceptible. If the 
disappearance of the pulse during gradually increasing pressure is 
chosen as a criterion for the systolic level, instead of its reappear- 




ance after obliteration during a falling manometrical pressure, 
higher values (3 to 10 mm. Hg.) will be obtained. The return of 
the pulse after obliteration is also a much more sudden and well- 
marked phenomenon than the disappearance during an increasing 
pressure, and the exact moment at which it occurs is much easier 
to determine. It is essential, however, that the pressure should 
be allowed to drop slowly and steadily, otherwise 1 the first few small 
beats will not be appreciated. A much more important reason 



PALPATdin' METHOD 



67 



lies in the fact that the lower reading is also somewhat nearer the 
actual intra-arteria] pressure, because we more or less counter- 
balance the overestimation caused by the resistance of the arterial 
wall and the tissues of the arm. More accurate readings will be 
obtained if the radial artery is palpated with the ball instead of 
the tip of the finger. The latter should rest against the overhanging 
cduc of ilif radius, thus permitting the application of a verj 
uniform pressure (Hirschfelder) (Fig. 13). 

The reappearance of the pulse below the point of constriction 
may be recognized by other means. Thus, if instead of the pal- 
pating finger a sphygmograph is attached to the \\ rist , or if a 
cuff communicating with some sort of recording device is substi- 
tuted, the return of the pulse can be made manifest. 




Radius c " 

Fig. 13. — Position of the finger in palpating the radial artery. 



B. Estimation of the Diastolic Pressure. — The estimation of the 
diastolic pressure was, until the auscultatory method was discov- 
ered and generally adopted, a more difficult and uncertain procedure. 
By means of the last-named procedure, however, we are now able 
to make readings which from the standpoint of accuracy and 
celerity compare very favorably with those employed for the 
systolic pressure. The estimation of the diastolic pressure is of the 
greatest importance and for general clinical purposes no examina- 
tion can be considered complete without it. 

The basis for all determinations of the diastolic pressure rests 



OS INSTRUMENTA L ESTIMA TION OF BLOOD-PRESSURE 

on the fact that when the pressure in the brachial cuff is at the 
diastolic level, the greatest oscillation in the caliber of that portion 
of the artery which lies beneath the cuff will occur. If the cuff 
pressure is higher, only the upper portion of the pulse wave will 
pass through; if lower, the artery will not completely collapse. 
Whichever the method of estimation of the minimal pressure 
employed, the end in view is always that of making manifest, in 
one way or another, the exact point at which this alternate 
maximum filling and collapse occurs. Thus by: 

1. Palpation (Strassburger). — The radial artery below the cuff is 
palpated between the finger and the radius, while the manometri- 
cal pressure is slowly increased. It will be noted that at a certain 
point, usually quite well marked, the pulsations suddenly become 
throbbing (knocking or bounding, "klopfend"), owing to a com- 
plete alternate distention and collapse of the artery. This phenom- 
enon occurs when the minimum pressure is reached. The first 
bounding pulse is to be chosen as the criterion (often this charac- 
teristic continues for some time during the rise of pressure). The 
method has been found very accurate when compared to graphic 
registration; the first bounding wave corresponding to the first 
full wave on the tracing (Gallavardin). Although this method has 
been highly recommended by Ehret, 1 who palpates the brachial 
artery immediately below the cuff, we cannot commend it; it 
requires long practice, and even one who is skilled in its performance 
is hampered by too much of the personal equation. 

2. Visualization. — With that pressure in the cuff at which the 
greatest arterial fluctuation occurs, the greatest oscillation will also 
be transmitted to the mercurial column. Hence observation of 
the lowermost point of the maximum mercurial oscillation was for 
a long time used as a criterion of the minimum pressure. Owing, 
however, to its great inertia, mercury is with difficulty set in motion 
by the compressed air, but once in motion its oscillation may be 
maintained or even increased by very slight pressure changes. 
Furthermore, many instruments were equipped with a U-shaped 
manometer so that the actual mercurial fluctuation was diminished 
by half. It has been partly as the result of this that so many 
different instruments have been placed on the market, although, 
of course, compactness, portability, and cost have also entered into 
the problem. 

The Stanton instrument owes much of its well-deserved popu- 

1 1'cImt cine einfache Best immungsmethode ties diastolischen Blutdruckes, 
MUnchen. med. Wchnschr., L909, No. 12. 



THE AUSCULTATORY METHOD 69 

larity to the fact that, being of the single tube type and well 
proportioned, it yielded large mercurial excursions. 

The maximum oscillation in other forms of apparatus, spring 
manometers (v. Recklinghausen), aneroids (Pachon, Rogers, San- 
born), is also used to determine the point of maximum arterial 
fluctuation. 

II. THE AUSCULTATORY METHOD. 

In 1905 Korotkow suggested the determination of blood-pressure 
by auscultation. Owing to its simplicity, celerity and accuracy 
this method has supplanted all others for clinical work. 

If, instead of palpating the artery below the compressing cuff, 
we apply the bowl of a stethoscope and listen, we will hear a vari- 
ety of sounds during the fall of the mercurial column. Five distinct 
'phases can generally be made out and quite clearly differentiated: 

(1) A sound not unlike the first cardiac sound. (2) This same 
sound plus a hissing murmur. (3) The murmur disappears and 
only the sound is heard. (4) The sound suddenly becom< 
much muffled. (5) The sound disappears. These phases occur 
while the pressure in the cuff is falling in the order given. 

The first sound or phase has been ascribed to sudden distention 
of the collapsed brachial artery, but more recent investigations 
have shown this explanation to be erroneous. In 1914 Macwilliam 
and Melvin 1 noted that perfectly well-developed and characteristic 
sounds were heard when the artery consisted merely of a tube in a 
compression chamber. In other words, the sound originated in the 
artery beneath and not beyond the cuff. More recently Erlanger, 2 
who has extensively investigated the subject, states that the sounds 
are due to a water-hammer action — the pressure exerted when the 
motion of a mass of fluid is more or less suddenly checked. 

"Under compressions which permit the pulse to determine rela- 
tively wide excursions of the arterial wall in the compression cham- 
ber, that is, under compressing pressures ranging from the systolic 
arterial pressure to, and even a variable distance below, the diastolic 
pressure, the volume of the compressed artery increases abruptly 
with each pulse. This permits a considerable volume of blood to 
enter the opening artery with a high velocity. The motion of this 
column of blood is, however, suddenly checked where it comes into 
contact with the stationary, or practically stationary, column of 

1 The Estimation on the Diastolic Pressure, Heart, 1914, v, 153. 

2 The Mechanism of the Compression Sounds of Korotkoff, Am. Jour. Physiol., 
1916, xl, 1. 



70 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

blood filling the uncompressed artery below. The water-hammer 
that is thus set into play distends the arterial wall at the point of 
impact with unusual violence. This distention sets the arterial 
wall into vibration and the sound is produced." The onset of this 
phase indicates the systolic pressure. 

The Second Phase. The addition of a murmur to the first sound 
is due to the formation of fluid veins, whirls, eddies, produced as 
the blood Hows past the constriction into the relatively dilated 
artery below the cuff. 

The Third Phase.- Disappearance of the- murmur is caused by 
sudden vibrations of the vascular wall produced by the increased 
volume of blood which, although diminished in rapidity of How, 
now reaches the artery at the point of auscultation. The cuff 
pressure being diminished, the water-hammer action is less marked. 
This phase is generally distinctly louder than the first. It corre- 

Release Pressure 




Clear & Soft 
Short Murmu 



Rising Pressure 
Fig. 14 

sponds to the stage of large oscillation in the graphic method, and 
its end occurs simultaneously with the Ehret phenomenon and the 
last of the maximal graphic waves (see Fig. IS). 

The Fourth Phase 1 — muffling of the sound — arises when maximal 
arterial filling and collapse no longer occur. According to Mac- 
william and Melvin, 2 the fourth phase owes its characteristics to the 
fact that external pressure has become insufficient to cause a flat- 
tening of the circular arterial tube. They believe that maximum 
arterial oscillation occurs, not as stated by Marey and generally 
accepted, at the point at which external pressure in the cufl" and 
internal pressure in the artery are exactly counter-balanced, but 
at the point at which external pressure is sufficient to distort the 

'This phase, not mentioned by Korotkow, was first described by Ettinger: Wien. 
klin. Wchnschr., L907, p. 992. 
^ 'l'lic Estimation >>r the I >iastolic Blood-pressure in Man, Heart, l'.U t, v, 153. 



THE AUSCULTATORY METHOD 



71 



arterial tube so as to produce a half-flattening of I he artery. Erlan- 
ger, however, found that "the maximal oscillation can be obtained 
;it a time when, during decompression the arterj has attained ;i 
'half -flattened' state onlj it' the pulse has an atypical form, such as 
probably could lie developed under artificial conditions only." The 
onset of this phase indicates the diastolic pressure.* 




Fig. 15. — The auscultatory method. 



TheFifth Phase — disappearance of all sound — occurs when normal 
arterial relations are again established. The onset of this phase 
is accepted by some authorities as indicating the diastolic pressure, 
although it seems well established that the beginning of the fourth 



1 Macwilliam, J. A., and Melvin, G. S.: The Estimation of the Diastolic Pressure, 
Heart, 1914, v, 153. 



72 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

phase should be chosen as the criterion. 1 In 118 cases in which 
both the fourth and fifth phases could be definitely identified it 
was found that the average difference between the two points was 
14 mm. Hg. 2 

It occasionally happens that the change from the third to the 
fourth phase is not clearly defined and it is sometimes necessary to 
make several observations before the exact point of change can be 
established. This is, however, not often the case among those who 
are accustomed to the auscultatory procedure. The identification 
of the onset of the fifth phase is much less readily established, and 
even when accomplished is subject to a much greater element of 
personal error. Some recent observations indicate that when we 
are confronted with sudden changes in pressure due to psychic 
influences (observations on students), the fourth phase is more 
consistently established, whereas among hospital patients the fifth 
phase shows less variability. 3 

The actual average duration of the different phases as measured 
in millimeters of mercury was found by Goodman and Howell 4 
to be 14, 20, 5, 6 mm. in the order given. These last-named authors 
opened up a very suggestive line of investigation in this field by 
measuring the actual duration of the different phases and their 
relation to each other under various pathological conditions. In 
cases of aortic regurgitation and hypertension, for instance, the fifth 
phase is persistent. (In aortic insufficiency a pistol-shot sound is 
often heard over the arteries when no pressure is being exerted.) 
Persistence of the fifth phase may also occur in hyperpyrexia, exoph- 
thalmic goiter, arteriosclerosis and other conditions. In failing 
compensation the second phase is said to be the first to show abbrevi- 
ation. A long third phase indicates a powerful systole. This phase 
is also lengthened in arteriosclerosis even in the presence of cardiac 
weakness. The length of the fourth phase increases when cardiac 

1 Lang and Manswetowa, in comparison with the Hurthle spring manometer, 
obtained closely corresponding readings by taking the auscultatory readings at the 
beginning of the fourth phase, Deutsch. Arch. f. klin. Med., 1908, xciv, 441. Fischer 
also believes that the beginning of the fourth phase represents the diastolic pressure, 
Deutsch. med. Wchnschr., 1908, p. 1141. Taussig, A. E., and Cook, J. E.: Determi- 
nation of the Diastolic Pressure in Aortic Regurgitation, Arch. Int. Med., 1913, 
xi, 542. Warfield, L. W.: Studies in Auscultatory Blood-pressure Phenomena, 
Jour. Am. Med. Assn., 1913, lxi, 1254. 

'Swan, .1. \V.: The Auscultatory Method of Blood-pressure Determination: A 
Clinical Study, Internat. Clinics, IV, Series 24. 

1 Kilgore, Berkeley, Howe, and Stabler: A Quantitative Determination of the 
Pel onal Factor in Blood-pressure Measurements by the Auscultatory Method, 
Arch. Int. Med., 1915, xvi, 927. 

*Tr. College of Physicians, Philadelphia, 1911; Am. Jour. Med. Sc, September, 
1911. 



THE AUSCULTATORY METHOD 



73 



weakness exists. 1 Atypical auscultatory findings are often asso- 
ciated with cardiac insufficiency (Krylow). to some apparently 
normal cases all the phases cannot be made out, but in the vast 
majority, although some may be brief, the five phases are distinctly 
demarcated. Variations in the strength of successive systoles are 
often better appreciated by auscultation of the partially compre "I 
artery than of the precordial "tonal arrhythmia." 



Arli it'll sound 



•LA 



ll.j. 122 



-^-^-wimwuij^^ 



Fig. 16. — Fast drum. Sudden decrease in size of pulse wave al -J. marking the 
change from clear, sharp tone to dull tone. 



Mj 
"Tv 



limn 



11 I I I . 



in 



Fig. 17. — Diagrammatic representation of the auscultatory phases (after Galla- 

vardin). /, arterial tone (muffled); //, tone and murmur; ///, arterial tone (loud 
and without a murmur) ;~IV, n milled sound. 





I I 



111 



III 



I I 



Fig. 18. — Showing the relationship between the oscillatory and the auscultatory 
phenomena (Gallavardin) . Here the end of the third phase is drawn as correspond- 
ing to the last large oscillation. 



In estimating blood-pressure by the auscultatory method any 
type of manometer — mercurial, aneroid, compressed air — may r be 
employed. 

As a general rule a long and intense murmur phase, beginning 
at a high pressure, points to a vigorous heart action. If it increases 
under exercise, we assume that the heart is using its reserve force. 
When the murmur phase disappears under light work cardiac 

1 Goodman and Howell: Univ. Penna. Med. Bull., 1910, xxiii, 465. 



74 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

weakness is implied, while the splitting of the tones of the first 
phase points to a dilated hypertrophy of the ventricle. If the 
sound or the murmur is subject to variations in duration and in 
intensity, cardiac insufficiency is predicated. The non-appearance 

of the murmur phase has a similar significance. 3 

Temporary Absence of the Second Phase. — It occasionally happens, 
as has beeB pointed out by Cook and Taussig,'- that the second or 
murmur phase may be very weak, short or entirely absent. This 
is especially apt to occur in cases of hypertension if the arm is kept 
compressed or the readings are not quickly made. Unless the 
height to which compression is primarily raised is controlled by 
palpation, auscultation may be begun in this silent zone. In such 
an event the third phase would be read as the systolic pressure, 
and an error of 50 mm. might be made. Such a mistake may be 
suspected if the pulse-pressure is found to be extraordinarily small 
will iout other evidences of cardiac weakness. 

The cause of this phenomenon may, as suggested by Erlanger, 
be due to the fact that a stasis of blood in the artery below the 
cuff, together with a high peripheral resistance, forces open the 
lower segment of the compressed artery. It has been shown experi- 
mentally that if the artery below the stethoscope be temporarily 
occluded while the compressing pressure remains stationary at the 
level of the first and second phases, the sounds become faint and 
often disappear. 3 

INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE. 
A. RIVA-ROCCI TYPE. 

The new Nicholson sphygmomanometer is a readily portable 
mercurial column instrument enclosed in a metal case. The lid 
when raised automatically locks in the upright position and acts 
as a support for the instrument (Fig. 19). 

We believe this instrument to be the best practical sphygmo- 

ma leter yet devised. It is small, accurate, readily portable 

and well constructed. Nicholson has also devised an even smaller, 
more compact, cheaper, and yet accurate instrument — the Princo 
sphygmomanometer which deserves an equal endorsement. 

l Tornai, -J.: Ueber d. diagnostisches Wert d. auskultatorischen Blutdruckmes- 
sungen, in besondere vom Standpunkt der Funktions-pruefung d. Herzens, Ztschr. 
f. Phys. u. <li:it. Therap., L909, xiii, 501 ot seq. 

'Auscultatory Blood-pressure Determination, Jour. Am. Mod. Assn., 1916, Ixviii, 
1088. 

'Erlanger, J.: Am. Jour. Physiol., 1916, ri, 113. 



tNSTRl \ii:\ts for usriMATixt; blood ri;i:ssi re 7." 




Fig. 1!*. — The new Nicholson sphygmomanometer. Showing the method of con- 
necting the unions A' and />" with the stopcock .1 and the connection /;. The 
needle valve C musl be closed, and the stopcock A open as shown in the ill'. 
To close the instrument remove the glass tube //. sliding it into the metal holder E. 

Fold the scale down and then remove the metal unions A' and />". The lid can 
then be made to close by firm pressure on its upper end. The lid cannot be closed 
until the stopcock .1/ has been turned at right angles to the tube, and when so 
turned no mercury can escape. When closed the instrument fits into a morocco 
case containing also the bulb and cuff, and can be carried in the pocket. 

Accuracy is assured: (1) by a millimeter scale, especially compensated for the 
lowering of the level in the mercury reservoir; (2) by the zero (0) point on the scale 
being adjustable to the mercury level, so that the readings are not affected by 
climate and temperature changes; (3) by the scale reading directly in millimeters 
of mercury, the primary standard, it does not have to he checked up; (4) by the 
use of a large column of mercury; there is no separation of the mercury, and oxida- 
tion and capillary errors are avoided; (5) by the use of a steel stopcock and flint- 
glass no amalgam is formed with the mercury, so no friction; (6) by a steel needle 
valve there is a perfect air release. The mercury remains clean owing to a new 
method of preventing powder from the rubber tubes being sucked into the mercury 
reservoir. 

Portability. (1) All parts are thoroughly protected by a metal case; (2) by a 
special stopcock no mercury can be lost; (3) by stopcock A one has an additional 
safeguard should the rubber washer in the pump leak slightly, until it can be 
replaced by a new washer. The mercurial column can be absolutely maintained 
by closing the stopcock. This permits of using the arm band to produce Bier's 
hyperemia. By inflating the apparatus to 50 to 60 mm. Hg. and then closing the 
stopcock A one can maintain the pressure for any length of time desired. This 
is impossible of attainment on any apparatus not having this stopcock. This 
is the only pocket sphygmomanometer which has this special feature. In addition 
to the above the apparatus is simple to operate, using a wide, soft cuff, and has an 
automatic catch on the lid which holds the instrument in the upright position when 
in operation. (Manufactured by the Precision Thermometer and Instrument Co., 
Philadelphia.) 



76 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

This instrument may also be obtained furnished with a Fedde 
indicator (oscillating index), which consists of a vertical tube con- 
taining a pith ball, the excursions of which during alternations of 
pressure are both free and extensive, thus affording signal aid in 
determining the diastolic pressure by the visual method (Fig. 53). 




Fig. 20. —Vertical cross-section of Nicholson's new pocket sphygmomanometer. 



Another instrument of the Riva-Rocci type, long familiar to 
American physician', is that of Janeway (Fig. 23). It is now 
supplied with a metal needle-valve pump instead of the rubber 
bulb depicted in the illustration. 1 

The Mercer sphygmomanometer is a mercury instrument the form 
and construction of which are shown in Fig. 24. The instrument 
may be clamped to a table or held in the hand while readings are 
made. The cuff and bulb are carried separately. 2 

1 Manufactured by Dressier-Beard Mfg. Co., 280 Second Avenue, New York. 
1 Manufactured by A. Kuhlman & Co., 203 Jefferson Avenue, Detroit, Mich. 



INSTRUMENTS FOR ESTIMATING BLOOD PRESSURE 77 

Leonard HUP has devised a compact and convenient form of 
mercury sphygmometer. It consists of a single graduated tube 
the base of which is sealed into a small reservoir in the lower end 
of which it opens (E). The tube leading from the cull* is attached 
to the other end of the reservoir, which contains the mercury. The 
chief advantages claimed for the instrument are: (1) The manom- 
eter being of the single tube variety halves the error of reading 





Fig. 21. — Nicholson's Princo sphygmomanometer. The instrument in a semi- 
folded and open position. A, terminal of tubing; B, socket for the same; C, stop- 
cock; D, needle valve; E, clamp level to set scale at proper mercurial level; F, mer- 
curial reservoir; G, hinge which permits folding of calibrated standard; H, auto- 
matic valve which permits folding of manometer tube and retains mercury when in 
transit ; J, scale folded ; K, tubing folded ; N, screw cap to permit removal of mercury. 



as compared with the U-tube type. (2) Owing to the capillary 
opening the mercury cannot spill. It can be carried in any position, 
requires no rubber caps or stopcocks. (3) Ready portability; no 
box is required; the wooden case, cuff and pump can be carried in 
a handbag (Fig. 25). 

H 

1 A New Form of Mercury Sphygmometer, British Med. Jour. .^February 19, 1910. 



78 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

Several inexpensive instruments of the Riva-Rocci type are on 
the market which, especially if the auscultatory method be em- 
ployed, will be found entirely satisfactory for clinical work. Among 




Fig. 22. — Faught's mercury sphygmomanometer showing relation of parts, metal 
pump, and special expansion tubing for infiator. 




Fig. 23. Janewaj 's sphygm 



INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE 79 

these the inst ruments of Linnell, 1 Kercher, 2 Cook, 3 Sahli, 4 Bruhns- 
Fahraeus 6 may be mentioned. (See p. 139.) 



300 



^ 



.■=■■' 



cLJ 



<=Q>= 




Fig. 24. — The construction of the manometer of the Mercer instrument. A U-tube 
manometer with the top of each limb of the U closed with a barometer kid gasket 
held securely in a metal socket. The gasket allows the air to pass freely but retains 
the mercury. The manometer is enclosed in an outer metal casing tube which is 
slotted and provided with a direct reading scale. The shorter limb of the U is con- 
nected with a slip socket in the bottom of the outer tube by a small metal tube as 
shown. Only glass and kid come in contact with the mercury. 



1 A Pocket Mercury Manometer, Jour. Am. Med. Assn., October 12, 1912, lix. 

2 Blood-pressure apparatus manufactured by Lander, Cleary & Co., Philadelphia. 

3 Cook sphygmomanometer manufactured b5 r the Kny-Scheerer Co., New York. 

4 Manufactured by Buchi & Sohn, Bern, Switzerland. 
6 Manufactured by Stein & Werner, Stockholm. 



SO INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

The Gartner tonometer 1 consists of small distensible rubber rings 
which are applied to the finger, and connected with a manometer. 
The finger is rendered bloodless and the point at which the blanched 
skin becomes rosy is taken as the criterion of the systolic pressure. 
This instrument yields variable amounts of error but is still occasion- 
ally employed in connection with brachial readings to determine 




Fig. 25. — Hill's sphygmometer: A, sphygmometer; B, case; 0, section of mercurial 
reservoir; D, brachial cuff; E, pump. 



the pressure ratio between large and small arteries, in the hope of 
thus throwing some light on the state of vascular tonus (Fig. 26). 

"The method of Gartner is open to the objection that the arteries 
of the fingers are probably small enough to participate directly in 
vasomotor changes. Therefore a rise of the general blood-pressure, 

1 W'icn. med. Wohnechr., 1899, xlix, 1412. 



INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE 81 

which in part is caused by constriction of the digital arteries, may 
be associated with a fall of pressure in the terminal phalanges. 
That this does occur is practically demonstrated by the fact that 




Fig. 26. — Gartner's tonometer. 



cold, which usually causes peripheral constriction with consequent 
rise of the general blood-pressure, seems to cause a fall of pressure 
as estimated by the method of Gartner." 1 

1 Erlanger: The Circulation, Jour. Am. Med. Assn., October 27, 1906. 



S2 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 




Fig. 27. — Bishop's blood-pressure apparatus. 

Legend for Fig. 28. 
Universal Bphygmomanbmetroscope. At Janowsky's Clinic in Petrograd the 
blood-pressure in the upper extremities is determined by comparison of the findings 
of five different apparatus. These include the Riva-Rocci cuff, the tonometer, the 
two spring manometers of Basch and the water manometer of Zipliaef-Janowsky. 
X. van Westenrijk, of Petrograd, has succeeded in combining these various apparatus 
in a single one in which one mercury manometer answers for all. It is arranged so 
thai i he zero point can bo adjusted, and it allows comparison of the findings with 
different technic and registration of the pressure up to 350 mm. Hg. The mercury 
tube R (Figs. 1 and 3) opens below into the reservoir R', the graduated scale (Figs. 1 
and I) being fastened within the mercury tube and the reservoir. The whole is 
mounted on a weighted wooden standard. The right-hand branching arm of the 
reservoir A" (Fig. 2) is connected with the tube which forks to the Riva-Rocci cuff 
K < Fig. 1), the Gartner tonometer ring D, the Basch contrivance for determining the 
in the capillaries /', the rubber bulb for determining the blood-pressure in 
G, and the rubber bulb // for increasing the pressure in the glass chamber 
F. All these are controlled with stopcocks in the tubes. The left-hand branching 
tube from the reservoir A" is connected with the rubber bulb A, which is compressed 
by a Bcrew lever to increase the pressure (Fig. 1) in the cuff and ring and also in the 
manometer. The tube />', with its two enlargements and capillary lumen (oscillom- 
eter) runs in the groove A", and is brought into connection separately with the cuff, 
ring, etc., on the other side of the reservoir A", by turning the stopcock C. 



INSTRUMENTS FOR ESTIMATING BLOOD-PRESSURE S3 




Fig. 2S 

The apparatus allows the Riva-Rocci cuff to be used for tonometry as well as in the 
usual manner. The illustrated description is published in the Mitteilungen der 
Gesellschaft f. innere Med., 1908, vii, 202. Universal sphygmomanometroscope, 
manufactured by Eberhard, Petrograd, Russia. 



84 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

What may be described as a home-made blood-pressure apparatus 
lias been devised by Bishop. Theaccompanying diagram is suffi- 
ciently explanatory to indicate the general principle upon which 
the instrument is based 1 (Fig. 27). 




Fig. 30. Hertz sphygmomanometer. 2 

For detailed description see L. F. Bishop: The Measurement of Human Blood- 

ixch. Diag.. April, L908. 
»Dae Neue Model] meines Blutdruckmessers, Wien. klin. Wchnschr., 1911, No 
,;7, p. 1306. Kolomoitzew (Munchen. med. Wchnschr., July 20, 1909, p. 1482), 
i obtaining figures within normal rangesjjwith this instrument, found an 
accurate accordance with Riva-Rocci reading in only 13 per cent, of the cases. 



COMPRESSED AIR MAXOME'I I l: 



85 



B. COMPRESSED-AIR MANOMETERS. 





Compressed-air instruments are small, light and compact. A 
small quantity of mercury or colored liquid is kept in the bulbous 
end of the glass tube. \\ hen pressure is raised, a drop of this fluid 
is forced up into the glass tube. This is 
simply used as an index l>\ means of 
which the height of the pressure can be 
read off. 

The Oliver Instrument. 1 Method. — Lay 
the instrument on a flat surface and lift 
the upper end of the manometer by the 
brass ring, at the same time opening out 
the hinged prop at the back to the ex- 
treme right-hand corner of the box. This 
places the scale at an angle of about 15 
degrees and facilitates observation. Tem- 
perature variations are compensated for 
by the vacuum which surrounds the 
pressure chamber. The scale is in milli- 
meters of mercury, having been stand- 
ardized. Any mercury remaining in the 
tube may be shaken down, as in a ther- 
mometer, when the box is closed. A 
modification of this instrument is made 
by Tech, of New York. The instrument 
is simple and compact. It consists of the 
usual cuff and inflation bulb. The man- 
ometer is of the compressed-air type, a 
drop of mercury being used as an index. 
It is open to the criticism, however, that 
the small scale with widely spaced grada- 
tions militates against accuracy. 

Hertz's Sphygmomanometer. — Method. — 
After application to the wrist as shown 
in the illustration, the cautery bulb / is 

tensely inflated, the clip d cutting off communication w r ith the cuff. 
When this is accomplished the clip d is opened and the droplet of 
mercury approaches the distal end of the manometer. The systolic 



Fig. 3 1. — The Benedick In- 
strument. Diagram showing 
the glass tube of the water 
sphygmomanometer: A, bulb 
partially filled with water on 
which pressure is exerted by 
a column of air in the tube 
leading from the cuff; B, level 
of water in upright calibrated 
tube C, which contains air 
above; D, bulb in the tube 
C, to contain the air as the 
water rises. At the top of 
the tube is a cock for closing 
the tube after the water is 
put in below. 



Manufactured by Dressier-Beard Mfg. Co., 386 Second Avenue, New York. 



86 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

pressure is read at the point at which the radial pulse disappears; 
the diastolic pressure, at that at which the pulse becomes dimin- 
ished in volume. 

Benedick's Air-water Sphygmomanometer 1 is calibrated in milli- 
meters of mercury. Water is poured into the reservoir until the 
points A and B are reached. The stopcock is then closed above D. 
The pressure in the cuff is exerted on the fluid at A and transmitted 
to B while the air in the column is being compressed. The bulb 



hi 

i 

i 

. | 

} 

i 

1 i 
# \ 


( 

m 

- 
* 

! 


i 


n ~ ■ 

i ^ - 


Vi' -N 


Kji 


•Sr' "^ 





Fig. 32. — Benedick's air-water sphygmomanometer. 

acts as a reservoir for the fluid, the bulb B for the air, allowing 
the liquid to rise the entire length of the tube in recording pressures 
up to 300 mm. Hg. Tbe two bulbs allow for a larger and more 
accurate scale than is the case where straight tubes are used. The 
metal T-tube with a stopcock and needle-valve escapement allows 
the air pump to be disconnected and controls the fall of pressure. 



1 A New Air-water Sphygmomanometer, Jour. Am. Med. Assn., 1911, 
Manufactured by Eimer & Amend, 205 Third Avenue, New York City. 



lxi, 1873. 



CHAPTER III. 

THE INSTRUMENTAL ESTIMATION OF BLOOD- 
PRESSURE (Continued). 

III. The Graphic Method of Estimating Blood-pressure.— If instead 
of employing the finger below the cuff in order to determine the 
presence and character of the pulse wave, a sphygmograph is 
substituted, one obtains a graphic tracing of the appearance, 
increase, maximum oscillation, and final disappearance of the 
pulse, which occurs while the pressure in the cuff is falling from 
above the systolic to below the diastolic pressure. Such a procedure 
has the advantage of furnishing a permanent record, and also of 
allowing one to judge more accurately the exact point at which 
the maximum pulsation is established. The graphic method is 
therefore employed where the greatest accuracy is demanded, as 
in experimental work. 

In the instruments of Erlanger, Uskoff, Muenzer, instead of a 
sphygmograph on the radial artery, the brachial pulsation of the 
cuff itself is transmitted indirectly to a kymograph. "Indirectly," 
because the pressure in the cuff, were it not "stopped down," would 
be too great for the delicate membranes connected with the tambour. 

The systolic pressure is determined by noting with a decreasing 
pressure the point at which the first full pulse wave is transmitted 
to the drum. While the cuff pressure is still above this level a series 
of small elevations often appear which are due to the impaction 
of the pulse wave against the upper margin of the cuff, the central 
portion of which still occludes the blood flow. 

The lower end of the maximum excursions is generally taken as 
an indication of the diastolic pressure because at this point there 
is just sufficient pressure in the cuff to cause a complete diastolic 
collapse of the artery, while at the same time permitting a com- 
plete distention during systole. Pressure on either side of the cuff 
being about equal, although alternate, the greatest oscillation of 
the interposed membrane occurs. Below this level the excursions 
grow progressively less because with the falling manometrical 
pressure less and less of the arterial pulsation is transmitted to 
the gradually loosening cuff. In some cases it is difficult to deter- 
mine the exact point at which the inframaximal pulsations begin. 



88 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

When the diastolic pressure is being estimated by the graphic 
method it sometimes happens that two regions of maximum oscilla- 
tion occur. "The first diminution in amplitude occurs apparently 
at the moment the blood begins to reenter the arm with considerable 
velocity. The amplitude again increases when the vessels of the 
arm become distended with blood." The second maximum is 
undoubtedly the minimum pressure (Erlanger and Hooker). 




Fig. 33.— Pulse tracing made with the Gibson instrument. Here the first full pulse 
wave (£) indicates the systolic pressure. It is the first wave which has overcome the 
pressure in the brachial cuff and reached the radial artery. Preceding the point S 
a number of small waves are seen which are produced by the impact of the pulse 
waves against the upper portion of the brachial cuff, a segment of the artery being 
still obliterated. Tracing taken by rapid inflation and gradual escape with quickly 
revolving cylinder. It shows systolic pressure to be 170; diastolic pressure, according 
to Gibson, 106 (D) ; and by Masing's method, 90 (/)'). (Tracing after Gibson.) 

Occasionally a successive series of maximum waves at about the 
diastolic level are observed. This is attributed by Sahli to two 
factors: (1) With increasing compression, when the minimal 
pressure is exceeded, the pulse wave undergoes a stasis underneath 
the (broad) cuff which increases the pulsatile excursions of the 
tonograph. (2) At the same time a continuously diminishing 
amount of the sphygmographic wave becomes available for trans- 
mission. These effects tend to counteract each other and the 
resulting waves will vary according to which of the two effects 
predominates. Another explanation is that the collapse of the 
artery being gradual, at first only that portion of the artery which 



GRAPHIC METHOD OF ESTIMATING BLOOD-PRESSURE 89 

underlies the centre of the cuff is compressed; some time is required 
before the whole segment is similarly affected (von Recklinghausen). 
According to this argument, with a rising pressure one should choose 
the beginning of the large oscillations as the diastolic criterion. 
This source of confusion may be obviated by the simultaneous 
employment of a brachial and a radial cuff, in which event the 
lower cuff will show a distinct oscillatory diminution the moment 
the diastolic level in the upper cuff is exceeded. 

If the pressure "be allowed to fall more slowly than in von 
Recklinghausen's experiments the maximum oscillations will be 
followed immediately by the abrupt diminution in amplitude — 
the diastolic pressure corresponds with the abrupt diminution in 
amplitude" (Erlanger). 

Gibson advised selecting the middle point of the greatest ampli- 
tude of oscillation as the diastolic point (Fig. 37). Strassburger 
takes the point at which the previous maximal oscillation begins 
to diminish under increasing pressure. Macwilliam and Melvin, 1 
who have investigated the relation of the diastolic pressure to the 
maximum oscillation, believe that the latter occurs not at the point 
at which internal and external arterial pressure are equalized, but 
when a " half -flattening" of the arterial lumen is brought about. 

Erlanger 2 has carefully re-investigated the significance of critical 
pressure oscillations by means of a circulation schema, in the hope 
of harmonizing the at present conflicting interpretations. As a 
result of these experiments he arrives at the following conclusions: 

"1. In the case of one and the same tube or artery the general 
configuration of the record of the compression pulses depends upon 
(a) the compressibility of the compression space and, if that is 
sufficiently small, upon (6) the phase of the pulse cycle in which the 
compression space is closed. The variations in configuration may be 
so marked under the different conditions as to show maximum 
oscillations at systolic, diastolic or mean compression pressures. 
Some of the discrepancies in the views held with regard to the 
significance of critical oscillations undoubtedly are attributable 
to the differences in the experimental conditions enumerated above. 

"2. The configuration of the oscillation record is influenced also 
by the extensibility of the artery, by the significance of the upper 
and lower conical closures of the artery relative to that of the 
completely occluded part between (length of artery), and by the 

1 The Estimation of Diastolic Pressure in Man, Heart, 1914, v, 153. 

2 Studies in Blood-pressure Estimations by Indirect Methods, Am. Jour. Physiol., 
1916, xxxix, No. 4. 



90 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

relation of the volume of the undistended bore to that of the dis- 
tended bore of the artery in the compression chamber. 

"3. When the compression space is sufficiently large the com- 
pression oscillations are proportional to the volume changes of the 
artery produced by the pulse and to the compressing pressure. 

'1. The volume change with each pulse is then determined by 
tlir difference between the volume of blood in the artery under the 
compression chamber during diastole and during systole. 

"5. During decompression the diastolic volume increases con- 
stantly though along three successive gradients, each of which is in 
the main determined by a different process, namely (in the order 
of their appearance): (a) the descent of the upper conical closure 
of the artery, (6) the ascent of the lower conical closure, and (c) 
the filling of the intermediate segment of the artery to its undis- 
tended bore (at diastolic compression) and the subsequent stretching 
of the arterial walls at compression below diastolic pressure. 

"6. The systolic volume also increases constantly and along three 
gradients determined by the following processes respectively: 
(a) the descent of the upper conical closure, (6) the filling of the 
central segment to its undistended bore (at systolic compression), 
and (c) the subsequent stretching of the arterial waU. 

"7. The diastolic and systolic volume gradients are so related to 
each other that the compression oscillations determined by their 
separation in different stages of decompression, have the relative 
amplitudes usually seen in records of the blood-pressure made by 
the oscillatory method; though it is obvious that as a result of dif- 
ferences in the relative significance of the factors determining the 
systolic and diastolic gradients variations from the typical record 
must frequently occur. Thus the slight diminution in the amplitude 
of the oscillations frequently observed before the sudden diminution 
begins is attributable mainly to an increase in the influence of the 
lower conical closure of the artery. 

"8. However, under all circumstances, natural as well as artificial, 
a sudden increase and a sudden decrease in the amplitude of the 
oscillations, if present, indicate accurately the systolic and diastolic 
pressures respectively. 

"9. It is shown that with a pulse of the configuration of the 
arterial pulse the maximal oscillation must be and is recorded at a 
time when the artery is still collapsed in the diastolic phase of the 
pulse cycle by the pressure from without. The maximal oscillation 
can be obtained at a time when, during decompression the artery 
has attained the 'half-flattened' state (Macwilliam and Melvin) 



GRAl'll/c METHOD OF ESTIMATING BLOOD-PRESSURE 91 

only if the pulse has an atypical form, such as probably could be 
developed under artificial conditions only. 

"10. During decompression a slight How of blood, which soon 
becomes faintly pulsatile, begins about 1<» mm. of mercury above 
the compressing pressure at which a brusque pulse, undoubtedly 
marking the first opening oul of the artery from the 'collapsed' 
state, appears." 

If a tracing is taken from the artery below the seal of compres- 
sion a sphygmographic curve results. In such a curve the onset 
of the large waves is accompanied by a change in fin- form of the 
waves. At the upper systolic level of the large waves the pulse 
previously anacrotic, becomes katacrotic; at the lower level the 
diastolic wave falls away almost vertically instead of obliquely 
(von Recklinghausen). These facts furnish us with a further 
means of recognizing the diastolic pressure provided we are able 
to recognize the katacrotic notch. 

The diastolic pressure by the graphic method, a- shown by 
Midler and Blauel, may l>e as much as 28 per cent, too high. 
Although the artery at once increases its oscillations when the 
diastolic level is reached, it takes some time for a complete arterial 
collapse to be established. 

The systolic pressure cannot always he absolutely determined 
because of the primary small subsystolic waves due to concussion 
of the upper border of the cuff. The diastolic pressure cannot always 
be absolutely measured because (1) there is still a difference of 
opinion as to which criterion should be used (beginning, middle, 
or end of the large waves or the onset of the anacrotic notch), and 
(2) because it is not always possible to determine the exact point 
at which these changes occur. But since it is admitted that clinical 
blood-pressure readings are approximate estimations only, and not 
exact mathematical calculations, the results obtained will be suffi- 
ciently accurate for practical purposes. 

Since the foregoing lines were written, corroboration of the state- 
ments made has been furnished by the investigations of Kilgore, 1 
who showed that identical tracings made with the Erlanger appara- 
tus were very variously interpreted by different individuals, even 
by those who were familiar with the instrument and who were 
using the same criteria of the systolic and the diastolic pressures. 

Erlanger states that these discrepancies can be minimized if 
not actually obviated by (1) using as the systolic criterion the 

1 The Large Personal Factor in Blood-pressure Determinations by the Oscillatory 
Method, Arch. Int. Med., 1915, xvi, 893. 



92 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

change in form, with the paper moving at sufficient speed for this 
purpose; (2) by using the first consistent decrease in amplitude as 
the diastolic index; and (3) in doubtful cases controlling the read- 
ings made by the method of continuous escapement by readings 
made by that of intermittent escapement. 1 

C. INSTRUMENTS FOR GRAPHIC REGISTRATION. 

When using the graphic method, some sort of an automatic 
registering device should be attached to the instrument, for other- 
wise one is forced to mark by hand the various pressure levels on 
the moving paper while watching the fall of the manometer, a 
procedure which is always irksome and often inaccurate. Various 
devices have been employed to obviate this necessity by substi- 
tuting an automatic indicator which marks the varying height of 




Fig. 34, — The Jacquet sphygmotonograph. 

pressure upon the record. Thus in case of the sphygmotonograph 
of Jacquet 2 (Fig. 34) the stylet of a small metallic manometer 
communicating with the brachial cuff registers directly on the 
tracing. The beginning of the curve represents 50 mm. Ilg., and 
each elevation of 1 mm. on the tracing is equivalent to a pressure 
increase of 10 mm. Ilg. This device can be attached to the regular 
Jacquet cardiosphygmograph and has the endorsement of Gal- 
lavardin. It is open to the criticism which applies to all metallic 
manometers the necessity of standardization. 3 

Bingel 4 lias devised an instrument in which every pressure change 

1 Erlanger, .1.: An Analysis of Dr. Kilgore's Paper, >'t<-.. ibid., i>. 917. 

2 Manufactured by C. A- E. Streisguth, Strasburg, Germany. A. II. Thomas & 
f'o., Philadelphia agi 

■'■ Sill M-riii.'inii, who has studied the changes which occur in the diastolic portion of 
tin- Bphygmogram during an increasing cuff pressure, believes thai some deductions 
can thus be drawn concerning the amounl of vascular tonus. Neue Untersuchungs- 
ergebnisse bei d. Blutdruckmessung mittels dee Tonographen, Deutsch. A.erzte- 
Zeitung, May 15, L909. 

'Ueber Messung des diastolischen Blutdruckes beim Menschen, Milnchen, med. 
Wchnschr., L906, Jtxvi, 1246. Manufactured by Albrecht, Tubingen, Germany. 



INSTRUMENTS FOR GRAPHIC REGISTRATIOh 



93 



of 10 mm. is marked od the tracing by the interruptions of an 
electric current. This spacing is rather wide even for clinical 
purposes. 

The sphygmomanometer devised by G. A. (iil).s-iui ] (Fig. 36) con- 
sists of ";i mercurial manometer, the lumen of which is exactly 
that of the ordinary physiological kj olograph." The air contained 
in the armlet can be increased, and the pressure on the limb there- 
fore elevated, by means of a large syringe, and the pressure maj 
be raised quickly or slowly, according to requirements. By means 
of a valve the pressure may also be lowered quickly or slowly. 
A float rests upon the mercury, surrounded, as is usual in the 
physiological laboratory, by alcohol, and an uprighl rod of aluminum 
leads to a horizontal arm which write- on the revolving cylinder. 
In order to have the absolute zero, a fixed arm traces the abscissa 




Fig. 35. — Cross-section of the registering metallic manometer of Jacquet. 

upon the cylinder, which is driven by a clock-work placed hori- 
zontally, as in the instrument of Erlanger. The pulsations of the 
artery below the point of compression are recorded by means of a 
transmission sphygmograph. This consists of a tambour brought 
into contact with the brachial or radial artery, as may be most con- 
venient, by a pelotte resting upon the vessel. It is adjusted to the 
arm by means of a spring provided with a screw. This tambour 
is brought into communication by rubber tubing with another 
tambour, the movements of which are recorded on the cylinder 
simultaneously with the movements of the kymograph. The 
best tracing is obtained when the tambour in contact with the 
artery is larger than that connected with the recording lever by 



1 Quart, Jour. Med., 1907, i, 103. 



94 INS 77.' I MK.X TA L ES TIM A TION OF BLOOD-PRESSURE 

means of which the movements are amplified. The whole appa- 
ratus is shown in Fig. 36. 

"Iii using the instrument the pressure within the cuff may be 
raised gradually or quickly, the latter being the more usual course. 




Fig. 36. — Gibson's sphygmomanometer. The recording sphygmomanometer 
described in tin- text: 1, armlet; 2, manometer; 3, scale; 4, valve for regulating 
pressure; 5, clip, acting as a valve to syringe; 6, inflation syringe; 7, support for 
transmission sphygmograph; 8, pelotte; 9, screw for adjusting sphygmograph to 
artery; UK clip for arranging pressure; 11, recording lever of manometer; 12, 
weighted thread for adjusting lever; 13, tambour recording movements of transmis- 
sion sphygmograph; ///, arm marking abscissa ; 15, revolving cylinder; 16, dock-work. 



If it is slowly raised, the tracing of the kymograph shows at first 
a line of ascent with small oscillations, but as it rises the pulsations 
become more and more marked, and the excursion of the index 
more extensive, until a maximum point of amplitude is attained, 
when they begin to diminish and gradually disappear. Simul- 



INSTRUMENTS FOR GRAPHIC REGISTRATION 95 

taneously the transmission sphygmograph record a gradual 
diminution in the amplitude of the pulsations, which finally cea e. 
When all the movements of the kymograph, as well as of the sphyg- 
mograph, have come to an end, the pressure is allowed to tall by tin- 
escape of air from the valve, and the events which follow are the 
converse of those jusl described." Such a tracing is shown in Fig. 37. 
The manometer is of the double column (U-shaped) variety 
and in reading the record the height of tlical« • i a musl bedoubledj 
e. g. } actual reading 60 mm., corrected reading li'O nun. 




Fig. 37. — Tracing obtained by slow inflation and slow continuous escape The 
ascending curve shows the pressure to be ISO systolic and 120 diastolic. The descend- 
ing curve shows it to be ISO systolic and US diastolic. 



If the pressure in the cuff is allowed to fall continuously, the 
oscillating mercury acquires a progressively increasing momentum 
which tends to depress the lowest point of movement beyond its 
true level. This point is well illustrated in Fig. 38, a tracing taken 
by the method of intermittent escapement. In order to obviate 
this, Gibson advocates choosing the mean instead of the lowest 
point of the curve when reading the diastolic pressure. 

The advantage of this instrument over that of Erlanger lies in 
the fact that the height of the mercurial column is automatically 
recorded, and that the personal equation is entirely eliminated. 
Its disadvantage in relation to the former is due to the inertia of 
the mercurial column which renders it less sensitive to delicate 



96 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

pressure changes. A closely similar instrument has been devised 
by C. Singer, 1 which is better adapted to clinical purposes in being 
less bulky and heavy, without sacrificing accuracy. 

The Erlanger 2 sphygmomanometer is an instrument somewhat 
similar to that last described. Owing to its size and construction 
it is better suited for the research laboratory than for the hospital. 
It has the advantage of yielding permanent graphic records, but 
necessitates considerable skill in its employment. 




Fig. 38. — Tracing taken by rapid inflation and gradual intermittent escape, inter- 
rupted approximately after each descent of 5 to 10 mm. Hg. It shows a systolic 
pressure of 118, and a diastolic pressure of 74. The varying effects of inertia are to 
be observed, as described in the text. (After Gibson.) 



While somewhat complicated in construction it differs from 
other instruments of this type chiefly in its method of recording 
pulsations. A U-shaped manometer connects by means of a four- 
way tube with (1) the arm cuff; (2) a special stopcock; (3) a rubber 
bulb enclosed in an outer glass bulb. The latter is interposed in 
order to reduce the pressure between the cuff and the delicate 
tambour. Records are made on smoked paper on a kymographion 
by means of an aluminum needle (Fig. 39) . The pump consists of 
a Politzer bag, and heavy, rigid tubing is employed. 

1 A Clinical Apparatus for Obtaining Graphic Records of Blood-pressure, Lancet, 
February 5, 1910, p. 365. Manufactured by Hawksley & Son, London. The instru- 
ment fits into a case 14§ x 5 x 4 inches; the cuff is carried in the cavity of the cylinder. 
The tracings are made with ink pens upon white paper. 

2 Johns Hopkins Hosp. Rep., 1904, xii, 62. 



INSTRUMENTS FOR GRAPHIC REGISTRATION 97 




Fig. 39. — Erlanger's sphygmomanometer. 



98 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

Some little time is required to make the records and considerable 
familiarity with the instrument is necessary, but graphic records 
eliminate subjective errors. It can be obtained with polygraphs 
attachments and used to make pulse tracings, but is, so far as the 
blood-pressure is concerned, not automatically recording, i. c, the 
height of the mercurial column must be observed and recorded 
by the operator while the tracing is being made. 

The systolic readings obtained with this instrument average 
5 nun. higher than with the Riva-Rocci method with a broad cuff. 
The diastolic readings correspond within a range of from 5 to 1 5 mm. 




Fig. 40. — The Uskoff sphygmotonograph. 

The Uskoff 1 sphygmotonograph (Fig. 40) was devised with the 
intention of supplying a portable instrument which could be used 
both for blood-pressure and for pulse tracings. The latter function 
it excellently fulfils, furnishing good simultaneous tracings of the 
brachial artery and any one other desired pulsation, and requiring 
practically no adjustment. 



i Der Sphygmotonograph, Ztschr. f. klin. Med., 1908, Ixvi, 1 and 2. Manufactured 
by E. Zimmerman, Leipsic. 



INSTRUMENTS FOR GRAPHIC REGISTRATION 99 

Blood-pressure tracings taken with tins instrument and auto- 
matically registered by an extremely ingenious escapemenl device 
are for two reasons not satisfactory. (1) Owing to the mallness 
of the opening which connects the interior of the glass bulb with 
the atmospheric air, large pulsations will transmit relatively more 
of their movement to the tambour than is the case with small 
pulsations. As a result of this, neither the sudden change from 
large to small pulsations (diastolic pressure . nor ye1 the change in 
the type of the individual waves \\ Inch should appear at this point 
(see p. 91) arc demonstrable (Staehelin and Faustus 1 ). (2 The 
rubber, glass-enclosed balloon exerts variable degrees of tension 
for increasing increments of pressure, largely owing to the effect 
of the silk netting by which it is surrounded | Erlanger 2 . 

The author, who has used this instrument in practice for i 
years on account of its other excellent features, having long 
become convinced of the inaccuracy of the blood-pressure tracings, 
has employed it with entire satisfaction as a simple manometer 
in connection with the auscultatory method. The driving mech- 
anism for the tracing is now furnished with two speeds, and a roll 
of smoked paper 25 meters in length, thus eliminating two of its 
early shortcomings. 

The Uskoff sphygmotonograph simultaneously records the 
following: 

(a) Blood-pressure in millimeters of mercury. 

(b) Carotid pulse (or jugular pulse or apex beat . 

(c) Arterial pulsation from the upper arm (brachial) at varying 
pressures (systolic and diastolic). 

(d) Time in one-fifth second. 

In other words, there are four tracings upon the paper, three of 
which are fixed by the limits of the apparatus, i. e., blood-pressure 
in millimeters of mercury, arterial pulsations at various pressures 
and time tracing, while the fourth record may be taken at pleasure 
from either the jugular vein, carotid artery or apex beat. 

Method of Operation. — The cuff M is attached in the usual manner 
to the upper arm and pressure applied by means of the bulb B until 
the pulse disappears. The pressure thus applied is first transmitted 
to the mercury manometer Q, lifting the perforated float as the 
mercurial column rises. At the same time it is transmitted to the 
rubber bulb enclosed in the glass bulb G which is in air-tight con- 

1 Das Verhalten des Blutdmcks beim Menschen wahrend der Erholung von 
Muskelarbeit, Ztschr. f. klin. Med., Ixx, 444. 

2 Criticism of the Uskoff Sphygmotonograph, Arch. Int. Med., 1912, ix, 22. 



100 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

nection with both the cuff and the manometer. With the handle 
of the cock H in the vertical position, the air in the glass bulb is 
expelled through the cock K 2 which is automatically opened at 
the same time as K 1 . 

When the pulse has, by application of sufficient pressure, dis- 
appeared the cock H is turned in the direction of the arrow, which 
movement connects the glass bulb G with the outside air through 
an exceedingly small opening, and the pulsations appear because 
air-pressure in the cuff and manometer is thus slowly relieved 
through the valve V and is divided between the rubber bulb and 
the air in the glass bulb G. The pulsations are at the same time 
transmitted from the air in the glass bulb G by means of the third 
tabulature in cod nection with the indicator to the tracing paper. 




Fig. 41. — Tracing of blood-pressure made with the Uskoff apparatus. The upper 
tracing (A) represents the pressure in millimeters of mercury, and the tracing is made 
while the pressure is reduced from 200 mm. to 50 mm., each vibration representing 
2 mm. of mercury column, with the one vibration, omitted every 50 mm. The second 
tracing (B) represents one taken from the carotid artery and recorded by indicator 
2. This indicator may be used to record either the apex beat or the jugular or other 
vein pulsations at will. The third tracing (C) is the sphygmotonogram or the tracing 
of the arterial (brachial) pulse under a falling pressure. With 200 mm. of pressure 
this indicator traces a straight line because of the total obliteration of the pulse. 
At 162 mm. of pressure the pulse reappears and at 92 mm. of pressure has reached 
the lowest point of maximum oscillation. If the float on the mercury column con- 
tinues to sink, the internal pressure is shown to be greater and the vibrations become 
smaller and smaller because of the elastic layer between the cuff and the artery, until 
it disappears entirely. This tracing taken under diminishing pressure constitutes, 
therefore, an accurate record of both the diastolic and systolic pressure. 



The pressure arising from compression of the rubber bulb B 
is also transmitted to two small outlets confronting each other 
on the top of the manometer, between which openings the per- 
forated float passes as it rises and falls on the mercury column. 
The small holes in the float are arranged 1 mm. apart with out- 
standing marks. The 50 mm. gradations are indicated by the 
omission of 1 mm. The passage of the air current through the small 
openings and through the corresponding perforations in the float 
operates indicator 3, and thus graphically records the actual press- 



INSTRUMENTS FOR GRAPHIC REGISTRATION 



101 



ure in millimeters of mercury at any moment throughout the 
operation. 

Another instrument of the graphic type is that of Silbermann 1 
(Fig. 42). It is comprised of a radial and a brachial cuff, a mercury 
manometer, float, revolving drum for smoked paper, and an auto- 
matic registering device. The latter consists of a vertical arm 
from which comb-like projections extend. These projections are 
regularly spaced at intervals corresponding to 5 mm. Hg. in the 
manometer. When the kymographion revolves a series of parallel, 




Fig. 42. — Silbermann's tonograph: B, brachial cuff; D, radial cuff; R, radial 
pulse recorder; T, time marker; F, float, indicating height of mercury in manometer; 
C, comb to mark 5 mm. spacings on kymograph; M , driving mechanism. 

horizontal lines — like a ruled page — are drawn on the smoked 
paper upon which the sphygmographic tracing is recorded. These 
parallel lines take the place of a scale on the manometer. The 
instrument is also supplied with a time marker, recording fifths 
of a second, and the driving mechanism with two speeds. 

Method. — -The brachial cuff B is applied to the arm, inflated 
just enough to bring the pressure level in the manometer on a 



1 Der Tonograph, Med. Klinik, August 30, 1908, No. 35, p. 1347. 
by Oehmke, 21 Luisenstrasse, Berlin. 



M anuf actured 



102 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

level with the first tooth of the comb, and then clamped off. The 
heavy, double cautery bulb is now inflated to its maximum capacity 
so that when the clamp is released after the kymograph is set in 
motion a steady and continuous rise in manometrical pressure 
will result. The radial cuff D, consisting of a small rubber capsule 
held in place by a strap, can be brought under different degrees 
of tension by means of a screw. When applied, this is so adjusted 
as to produce the maximum radial oscillation. It is used as an 
indicator of the levels at which with a rising pressure (1) the last 
pulse wave traverses the brachial cuff (systolic pressure); (2) the 
first maximum oscillation occurs (diastolic pressure). Readings 
obtained with this instrument are from 4 to 5 mm Hg. lower than 




Fig. 43.— -Tracing made with Silbermann's tonograph showing systolic pressure, 
118 mm.; diastolic pressure, 65 mm. 



with the Riva-Rocci method, discrepancies which result from the 
weight of the float and the friction produced between the float 
recorder and the smoked paper. As this error is a constant one 
the author suggests setting the abscissa line on a level with the 
second tooth of the comb (Fig. 43). 

Another graphic instrument has been devised by Brugsch. 1 It 
consists of a U-shaped manometer and a revolving drum covered 
with white paper ruled in centimeter squares, which can be set 
at any level. A registering float superimposed on the mercurial 
column transmits its height and pulsations directly to the drum. 
The latter is set at such a level that the abscissa of the centimeter 

1 Zur Frage der Sphygmotonographie, nebst Beschreibung eines neuen Sphygmo- 
tonographen, Ztschr. f. Exp. Path. u. Therap./ May 30, 1912, xi. 



Instruments for graphic registration 



103 



ruling and the zero point of the mercury correspond. Thus the 
actual height of the tracing above the base line, multiplied by 2 
(U-shaped manometer) gives us the correct reading. The brachial 
pulsations are transmitted by means of rubber tubing to a piston 
recorder and inscribed by means of ink pens upon the drum below 
the pressure curve (Fig. 44). 

A more elaborate and complicated instrument, based on the 
Erlanger principle, is the sphygmoturgograph of Muenzer 1 (Fig. 
45). The tubing S connects pump P with cuff M and is inter- 
rupted by stopcock h to prevent communication with the glass- 




Fig. 44 



— Brugsch's sphygmotonograph. 



enclosed balloon B, until this is desired. The tubing T, connects 
the balloon with the tambour. When air is pumped into the system 
it reaches the manometer St, the cuff M and the balloon B. With 
the cuff applied to the arm and sufficiently inflated, the cock h 
being closed, the pulsations are transmitted from the cuff through 
the balloon to the kymograph upon which they are recorded. The 
kymograph is supplied with two speeds — a slow one for blood- 
pressure tracings, a rapid one for pulse tracings — and a time marker. 

1 Apparat. z. objektiver Blutdruckmessung, etc., Miinchen. med. Wchnschr., 
1907, xxxvii, 1809; also Ueber Blutdruckmessung, Ztschr. f. exper. Path. u. Therap., 
1907, iv. 



104 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

In order to obtain the greatest and most accurate oscillations it is 
necessary to close both the cocks h and h' in order to exclude the 




Pig. 1"». — Muenzer's sphygmoturgograph. 




In.. Hi. — Turgo 



(Strauss-Fleischer.) 



LXSTh'l \ii:\ts mi; GRAPHh REGISTRATIOh 



Hi:, 



pump and the manometer, since in recording the pulsations only 
i he cuff and the balloon are necessarj . 

A somethat similar instrumenl has been designed by Fleischer,* 
who, however, instead of using the glass-enclosed balloon to 
diminish the force of the pulsations between the cuff and the tam- 
bour, lias constructed a device consisting of a metal cylinder M 
enclosing a celluloid cylinder I Sch I Boated on a la-, er of oil P . The 
air enters Prom the cuff through the tube r and finding no means 





ammaauamu/w^^ 



Fig. 47. — A, pen used for recording oscillations; B, tracing made with the Brugsch 
apparatus. (Brugseh.) 

of escape imparts its pulsations to the counterweighted lever G at 
the point A, whence a wire (D) again transmits the motion to the 
aluminum recording needle S. (Figs. 48 and 49.) 

The cuff shown in the accompanying Fig. 49 is used for the 
transmission of the pulse. It consists of a metallic cylinder L, 
the upper closed end of which is perforated by a tube which connects 
with the polygraphic tambour. Its lower end is closed by means 



1 Ueber turgotonographisehe Pulsdruckbestimmung, Berl. klin. Wchnschr., 1907, 
No. 35, 1108. 



106 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

of a "lense" consisting of a rubber capsule G filled with glycerin. 
The cuff is held in place by the straps R and its pressure can be 




Fig. 18. -Strauss-Fleischer device for damping the force of the pulse wave. 

adjusted by the thumb-screw Sp. With this cuff tracings can be 
made of most of the superficial arteries, including the digital and 
temporal vessels. 1 




In.. 19. Cuff used with Fleischer instrument. 



Bu88eniu8'8 instrument for the graphic registration of the blood- 
pressure ingeniously eliminates the necessity of a driving mech- 
anism for the strip of smoked paper in the following manner: A 
narrow strip of paper supported in an upright slot, falls by gravity 



Zur Methodik der P 



ireibung, Beri. klin. Wchnschr., L909, rivi, 2141. 



ixsriu mk.xts F(H{ dh'M'Uic REGISTRATIOh K)7 




Fig. 50. — Bussenius's sphygmotonograph. 



108 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSl RE 

pasl the oscillating tambour. Hie descent of the strip is delayed 
by the displacement of glycerin around a metallic plunger, which 
is 30 graded that the strip will fall 1 em. per second. Both systolic 
and diastolic pressures cau be estimated with this instrument; in 
fact, two tracings may be made consecutively on the same strip 
and used to control each other (see Fig. 50). It is merely essential 
that the beginning of the tracing corresponds with mm. pressure 
in the manometer. 1 

Wybauw's instrument- is essentially a modification of Erlanger's. 
He, however, uses a divided cuff (4 and 9 cm. broad) which yields 
a more accurate systolic reading, since the impactions of the pulse 
wave against the upper part of the cuff are not transmitted to the 
tambour. The height of the pressure is not automatically recorded. 

IV. Visual (Oscillatory) Methods. — Instruments of this type are 
constructed in association with different kinds of oscillating devices 
which indirectly magnify the fluctuations of the mercurial column, 
or otherwise render the pulsations of the cuff more readily percep- 
tible. The oscillatory method is more satisfactory for the deter- 
mination of the diastolic pressure than the method of palpation, 
but less so than that of auscultation. 

D. OSCILLATORY INSTRUMENTS. 

The instruments based on this method may be divided into : (I) 
Those which register the height of the pressure, and the degree 
of excursion by different devices. (II) Those which indicate these 
two factors upon the same dial. The former usually render too high 
systolic readings. The diastolic pressure as indicated by type II is 
practically similar to that obtained by palpation. In type I the 
readings are somewhat higher. 3 

Class I. — The apparatus of Bing 4 (Fig. 51) consists of a man- 
ometer, pump, two cuffs and a colored liquid indicator somewhat 
similar to that devised by Pal 8 (Fig. 52). Here the lower cuff b, 
substituting the finger in the palpatory method, transmits such 
pulsations as pass the upper cuff a to the colored oil droplets in 
the indicator v. The pressure on either side of the oil droplets 

1 Manufactured 1a \\ . Oehmke, Berlin. 

! Graphische BlutdruckbestimmungeE bei unregelmassiger Herzwirkung, Ztschr. 
f. k 1 i i , . Med., 1911, lxxiii, 204-220. 

< Sordier and Rebattu: Arch. d. mal. du cceur, 1911, iv, 737. 
«Ein Apparat. z, Messung dea Blutdrucks bei Menschen, Berl. klin. Wchnschr., 
L907, No. 22; Blutdruckmessungen bei Menschen, Berl. klin. Wchnschr., 1900, No. 52. 
\,\w Sphygmoakop. z. Bestimmung des Pulsdruckes, Zentralbl. f. inn. Med., 
I ebruary, L906, No. L5. 



OSCILLATORY INSTRUMENTS 



III') 



being equalized, a very slighl pulsation in the cuff produces an 
extensive oscillation in the sphygmoscope. 




Fig. 51. — Bing's sphygmomanometer: a, mensurating cuff; b, occlusive indicating 
cuff; c, sphygmoscope; d, control value; e, pump; /. manometer; g, manometer 
escapement; h, sphygmoscope escapement. 




Fig. 52. — The sphygmoscope. (Pal.) 



110 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

The values obtained average 10 mm. higher than with the Riva- 
Rocci method, chiefly owing to the fact that in the last-named 
procedure peripheral contraction of the brachial artery may cause 
a local elevation in pressure without affecting the rest of the 





IMPROVEMENTS FOR 
FACILITATING THE TAKING OF 
MINIMUM DIASTOLIC PRESSURE 



TO CUFF 
-> VENT 



WTO COMPRESSION DULD 



In.. 53. Fedde's oscillometer. This instrument has been modified by It. L. 
Hoobler \>y using two cuffs with a stopcock connection between them, in circuit with 
the pith-ball indicator. This permits the reading of the systolic as well as the diastolic 
pressure, and yields better results in infants (Nicholson). This oscillatory device 
may In- used in conjunction with many types of instruments. It is furnished (at an 
extra cost) with the Nicholson and the Faught sphygmomanometers. 



OSCILLATORY INSTRUMENTS 



111 



systemic circulation. This factor is said to be obviated in the 
Bint;- apparatus by the second nil!.' 

The Sphygmoscope (Pal). The capillary tube C-C, containing 
a lew drops of colored petroleum, communicates with the tube 
A-B, the left arm of which i.l-//i is smaller in caliber than the 
right (//-/>). .1 is a two-way <-(»ck enabling communication to 




Fig. 54. — Widmer's oscillometer. 



be established (through 8 and 4) with two manometrical cuffs, 
e. g., one on the arm, another on the finger. B is an escapement 
cock. The tube 2 communicates with a manometer, while 1 is 
connected with the pump (Fig. 52). 

1 v. Werth has devised a somewhat similar instrument, equipped with an oscillator 
which transmits the radial pulsations from a rubber glycerin-containing pelotte 
which can, however, only be used for the systolic oscillations. Ueber d. Messung d. 
Systolischen Blutdrucks auf Optischen Wege, Mtinchen. med. Wchnschr., 1910, 
lvii, 12S6. Manufactured by Oehmke, Berlin, Luisenstrasse, 21, N. W. 



1 1 2 INSTRUMENTAL ESTIMA TIOX OF BLOOD-PRESSURE 

Method. — After the pressure has been raised in the cuff, // is 
turned 45 degrees, thus closing all communications through the 
four-way cock, whereupon oscillations of pressure are manifest in 
the capillary tube C-C. 

Milliner's Oscillomanometer. — The first full oscillation (systolic 
pressure), and the maximum oscillation (diastolic pressure), are 
indicated upon the graduated scale, while the actual pressure is read, 
from the mercury manometer 1 (Fig. 54). 

Another instrument based on the same principle is the "sphygmo- 
signal" of Vaquez, 2 Here again two cuffs are employed, but with 
a metallic manometer and a different form of indicator (Fig. 55). 




Fig. 55. — Vaquez's sphygmo-aignal. 

E. ANEROID INSTRUMENTS. 

Class II. — The most accurate aneroid instrument at present 
available is unquestionably that of Pacho?i. z It has recently been 
highly commended by Bachmann, 4 who has made extensive studies 
regarding its accuracy. 

"In estimating the systolic pressure it is customary to observe 
the disappearance of the arterial pulsation at the radial (method 
of Riva-Rocci), occasionally at the brachial below the cuff, at 

1 Manufactured by W. Oehmke, Berlin. 

- For further description see Vaquez: Soc. de Biologie, 1908. 

1 Oscillometre sphygmanometrique a grande scnsibilite et a sensibilitc constante, 
Comptes rendus de Soc biol., lxvi, 776; also Paris Medicale, 1911, xxxi, 122. 
Manufactured by C. Verdin, rue Linne 17, Paris. A. H. Thomas & Co., Philadelphia 



*The Measuremenl <>f the Arterial Tension in Man, New York Med. Jour. 
February I, 1911. 



ANEROID INSTRUMENTS 113 

any rate always at some distance from the point of compression. 
This method of applying Marey's principle is essentially faulty 
and the results obtained arc necessarily erroneous. Indeed, it can 
be shown that while the pulse lias disappeared at the radial there 
is a pronounced pulsation in thai portion of the brachial arterj 
under compression. Pachon, who demonstrated this fact l>\ mean- 
of his instrument (to he described present 1\ ) and l>,\ tlie plr gmo- 
signal of Vaquez, gives the following theoretic explanation of In 
experimental finding: 

"The pulse wave has its origin in the contraction of the ventricle 
and represents a certain amount of kinetic energy. This wave 
of pressure spreads from the root of the aorta to the end of the 
arterial system and in so doing loses energy little by little, owing 




In.. .")(>. — The Pachon sphygmometric oscillometer. 

to friction against the sides of the vessels. As the resulting dis- 
tention of the arterial walls is normally extremely slight (Poiseuille), 
very little external work is performed by the pulse wave. If, 
however, a segment of an artery is compressed so that a portion 
of its internal pressure is counter-balanced, that segment will yield 
to a greater extent to the distending force of the pulse wave and 
the vessel wall will begin to move. In other words, external work 
will be done. The compression may be such that the extent of 
the movement of the vessel wall (hence the amount of work done 
by the pulse wave) will exactly balance the amount of energy 
possessed by the wave. At this moment the pulse wave is entirely 
utilized in performing mechanical work; it is therefore absorbed at 
this point and no pulsation can be felt below it. The blood flow, 
however, has not been interrupted, the intermittent flow has merely 



114 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

Urn changed into a continuous one. This explains why wide cuffs, 
with a larger area for the absorption of the pulse wave, give lower 
figures than narrow ones. It serves to explain also why the arterial 
pressure in man appears so low in comparison to that observed in 
the other mammalia. Benczur reached practically the same con- 
clusions by the combined use of the Recklinghausen and Gartner 
instruments" (Bachmann). 

Marey's principle for the determination of the minimum or 
diastolic pressure has been more correctly applied, in that the 
oscillations of the compressed artery are transmitted directly to 
the instrument and their amplitude noted. As stated by Pachon, 
however, the instrument which is to reproduce these pulsations 




Fig. 57. — Diagram showing the relation of the essential parts of Faction's sphygmo- 
meter: oscillometer. (After Pachon.) B is a rigid metallic box hermetically sealed and 
containing in its interior an aneroid drum (a) with which is connected the lever n. 
M is an aneroid manometer which indicates the level of the pressure in the entire 
system. The box, manometer, aneroid drum a, and the cuff are normally in free 
communication by means of the tubes d, e, f. The pressure can be raised in the 
system by means of the pump P; it can be lowered by allowing the air to escape by 
unscrewing the valve s. The cuff and the aneroid a can be cut off from the rest of 
the apparatus by compressing the rubber tube d by means of the compressor c 
(called separator by Pachon). (Bachmann.) 



must have both a great and a constant sensibility. The mercury 
manometer has naturally a constant sensibility, but owing to the 
inertia of the mercury this sensibility is but slight, surely not 
sufficient to enable one to compare differences in the amplitude 
of oscillations at various levels of pressure. Everyone who has used 
the mercury manometer for the determination of the diastolic 
pressure is impressed with its imperfections for this purpose. A 
few investigators have sought to overcome this defect by placing an 
elastic bag in connection with the cuff, through which combination 
the arterial pulsations are taken up and transmitted by appropriate 
means to a tambour to be magnified and graphically recorded 
(Erlanger, Uskoff). The first objection to this method is that the 



ANEROID TNSTRl WENTS 115 

bag cannot be made ensitive on accounl of the relatively high 
pressure to which it must be subjected. The second objection is 
that such a bag has no1 a constant sensibility a1 various pressure 
levels. The amplitude of its oscillations will be smaller the greater 
its state of tension (distention), the force of the oscillal ions remain- 
ing the same. It will therefore lead to error to compare thi ampli- 
tude of oscillations obtained at various pressure levels. 

All these objections have been removed in the simple and ingen- 
ious instrument devised recently bj Pachon. The main features 
in the const met ion of this instrument, which he names a sphy ^mo- 
metric oscillometer, can besl be undersl I bj reference to Fig. 57. 

'The position of the aneroid a is in the interior of the box, and 
the free communication of the interior of the same manometer 
with the box and the cuff have solved the problem of devising an 
instrument which would have both a greal and a constant sensibility 
at any pressure level. By reason of this arrangemenl the same 
pressure is exerted at all times on the externa] as on the internal 
surfaces of the drum a; hence this drum is always in a position of 
rest or zero tension, except w hen by compressing c the cuff is placed 
in direct communication with the interior of the drum and any 
change of pressure within the cuff may then act upon it. These 
changes of pressure due to the pulsations of the artery arc normally 
very slight, so that the drum a could be made of relatively thin 
metal, hence very sensitive. This sensibility will always be the 
same, no matter what the level of the pressure around the arm may 
be, since it always takes up the pressure changes in the cuff by 
starting from a state of no tension. 

"In using the instrument the cuft" is placed around the arm in 
the usual manner. Air is pumped into the system until the pressure 
is well above the normal arterial pressure. The amount of the 
pressure is read from manometer M. The observer now confines 
his attention to the manipulation of valve s and compressor c, 
using preferably one hand only in order to insure free opening 
of the tube d when valve s is opened and closed. If on compressing 
c the hand n does not oscillate, valve s is opened and the pressure 
allowed to fall one-half to one centimeter; c is again pressed upon 
and the hand n observed. This maneuver is repeated until oscilla- 
tions of the hand n to the extent of, say, one degree of the dial are 
shown. This moment indicates the return of the pulse at the point 
compressed, and therefore the maximum or systolic pressure there. 
This is read on manometer M. To determine the minimmn or 
diastolic pressure, the pressure in the system is lowered in the 



116 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

manner explained above and the eompressor c manipulated between 
each lowering of pressure; at the same time the hand n is observed 
and at the moment its excursions are greatest the level of diastolic 
pressure has been reached, and can be read on manometer M. This 
is the most satisfactory instrument I have seen for the determination 
of the diastolic pressure; the oscillations are large and the moment 
of greatest amplitude is clear cut, for both immediately before and 
immediately after this moment the oscillations are noticeably 
smaller." 




Fig. 58. — Diagram illustrating the construction of the Tycos aneroid. 

"The determination of the systolic pressure in such instruments 
is a vexed question. Erlanger obtains small pulsations with his 
instrument, as shown by the movements of the lever, before the 
true systolic level has been reached. This he attributes to the 
'hydraulic ram action 1 of the pulsating proximal stump of the 
artery against the edge of the cuff. Pachon now uses a cuff adapted 
to the wrist, where, on account of the small size of the vessels, and 



ANEROID INSTRUMENTS 



w: 



the fairly thick edge of the cuff, the danger of this source of error 
should be greatly minimized. The writer observed thai an oscilla- 
tion of the hand n, equivalent to one degree of the scale, indicates 
the return of the pulse at the point compressed, as controlled by 
the palpation of the artery under similar conditions. To determine 
this point a cuff is placed around the upper arm and one around 
the wrist. The two cull's are connected with the Pachon instrument 




ir ir 

Fig. 59. — Showing the construction of the Faught aneroid. 



by means of a Y-tube; a stopcock is placed in the course of each 
tube coming from the cuffs. A pressure is put around the wrist 
equal to the diastolic pressure at this point. When a pressure is 
applied around the brachial equal to the systolic pressure and the 
stopcocks and compressor suitably manipulated, no pulsation is seen 
at the wrist. The pressure must be lowered considerably around 
the brachial before a pulsation is indicated at the wrist. If now T 
the radial cuff is removed and the brachial systolic pressure esti- 



lis INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 



mated by the ordinary method of palpation of the radial artery, 
it will be observed that the pulse is felt when the pressure around 
the brachial is at the same level as when the indicator of the Pachon 
instrument showed an oscillation of approximately one degree, 
when it was in relation with the radial cuff. The following table 
will show the result of a few observations" (Bachmann): 



Systolic pressure in 
brachial artery i Pachon). 
Age. In mm. Bg. 

27 130 

26 1 25 

33 L30 



Pressure in brachial cuff 
at which pulse appears 

at wrist. 
(Pachon.) (Tactile.) 


Diastolic pressure 
at wrist 


1 1 15 
105 
110 


105 
105 
110 


80 
90 
90 




FlG. 00. — An aneroid instrument in us< 



The systolic readings with the "oscillometer" are from 20 to 
40 mm. Hg. higher than with the Stanton apparatus (Riva-Rocci 
method i. In the diastolic readings there is less discrepancy. This 
instrument is well suited to ward or office work. It is free from 
error due to personal equation, yields — especially for the diastolic 
pressure satisfactory results, and is quickly manipulated; but 
its weight militates against its ready transportation, and it is open 
to the objection which applies to all aneroids, namely, the necessity 
of occasional standardization. 

A number of compact little blood-pressure instruments fitted 
with aneroids are on the market. These instruments consist of a 

'Manufactured by G. P. Pilling & Co., Philadelphia. A somewhat similar 
instrument the Rogers "Tycos" sphygmomanometer is manufactured by the 
Taylor Instrument Co., Rochester, New Xbrk. 



I VEROID I \SThTMK.XTS 1 1!) 

chamber of corrugated metal which expands under pressure and 
Imparts its movement to a calibrated dial. Thej can be carried 

in the pocket and are free from all danger of spilling tin- mercurj , 
etc. Breakage is also less likely. They give readings sufficiently 
accurate for clinical work, I nit they have to be standardized from 
time to time, as they are apt to get out of adjustment. 1 Unless the 
readings obtained are occasionally checked up with .-in accurate 
manometer, one can never be sure thai the results are no1 erroneous. 
What has already been said regarding the size and character of 
the cuff of course applies equally to this type of apparatus. I 
have obtained very satisfactory service from the Sanborn aneroid, 
an instrument recently put on the market. 1 

Standardization of the Aneroid. The accuracy of the aneroid 
can be readily tested with an ordinary mercury manometer, if a 
three-way stopcock is used to connect the two manometers with 
a pump. The pressure is raised 5 nun. at a time and the readings 
indicated by the two instruments arc compared, thus showing the 
amount of correction which must he applied to the aneroid ;it a 
given level. 

The run Recklinghausen tonometer, 2 an instrument which ha-, 
found considerable favor in Germany, i- based on the principle 
"first introduced into physical science by Bourdon and later 
incorporated into the kymograph of hick, that if a very -hallow, 
curved, elongated air chamber is fixed at one end of the arc with a 
pressure apparatus, while the other is closed, any increase of pressure 
will be made manifest by a flattening or elongation of the arc, 
thereby imparting a certain movement to the end that is free. 
By a very simple device this movement of the air chamber is com- 
municated to an axis on which, guarded by a hair-spring, there 
is fastened a long needle whose tip is made to move along a gradu- 
ated scale previously standardized, the final figures being read 
off from the dial." The pressure which is supplied by a long-stroke 
bicycle pump is transmitted from a standard cuff to the dial, the 
graduations of which are equivalent to centimeters of water (Figs. 
61 and 62). 

It is for several reasons desirable that water should be adopted 
as a standard for measurement rather than mercury, and possibly 
this will sooner or later come to pass. First of all, pressure values 

1 Manufactured by the Sanborn Company, 79 Sudbmy Street, Boston, Mass. 
Sells for about one-half the price of other aneroid instruments. 

2 Unblutige Blutdruck Messung, Deutsch. Arch. f. exp. Path. u. Phar., 1906, lv. 
Manufactured by C. & E. Streisguth, Strassburg. A. H. Thomas & Co., Philadelphia, 

agents. 



120 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

can be directly translated into grams; second, water and blood 
have nearly the same specific gravity; so that calculations can 




Fig. 61. — The von Recklinghausen tonometer: A, cuff; B, pump; C, tonometer 
dial. 




readily be made as to differences in pressure at different levels 
of the hotly by simply measuring the difference in height in centi- 



AKHUOll) /AN/7,'/ l//.\ IS 



121 



meters, e. g., blood-pressure at cardiac level L40, at level of spleen 
140-20=120. 

Water having less inertia than mercury, and being used as a 
unit in many other connections, would undoubtedly be more de li- 
able as a standard for blood-pressure. Unfortunately, however, 
nearly all blood-pressure readings have been made with mercury, 
so that not only is nearly all the literature based on this standard, 
but we have come to think of blood-pressure in millimeters of 
mercury. A transposition of values from millimeters IIg. to 
centimeters ILO is not readily made without reference to a special 
table. This is one reason why the instrument has never found favor, 
in this country at least. Itisperhapsa pity, but we are confronted 




Fig. 63. — The new von Recklinghausen tonometer. 

by a fact. Another reason lies in the construction of the instrument. 
It measures tension by means of a metallic spring which perhaps 
even more often than in the case of aneroids requires "control" 
and occasional correction to insure accurate readings. 

The systolic pressure as recorded with this instrument is slightly 
above the actual pressure. The diastolic pressure, especially if 
the pulse-pressure be large, is too low. Strassburger 1 suggests that 
observations be based both on oscillation and on palpation; and 
further, that not only the extent of the excursion be used as a cri- 
terion of the minimum pressure, but also the point at which the 
needle begins to "hesitate" and to "tremble." He believes that 



1 Weitere TJntersuchungen u. d. Messung d. diastolischen Blutdruckes beim 
Menschen, Deutsch. med. Wchnschr., 1909, xxxiv, 56 and 100. 



122 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

in this manner the error due to the arterial elasticity (which varies 
in individuals, and for different degrees of pressure), as well as that 
resulting from partial loss of pulsation, due to imperfect transmis- 
sion from the cuff, may be mutually controlled. 

The Recklinghausen instrument has recently been modified, 
making it smaller in bulk (21 by 9 cm., weighing f kg.) and more 
readily transportable. It is also supplied in another modification 
for office use, with a good-sized compressed-air tank, so that very 
rapid inflation of the cuff is made possible by the release of a screw- 
valve, and repeated estimations may be made without renewing 
the air supply in the tank. Care must of course be exercised when 
releasing so high a pressure lest the limits of the instrument be 
overstepped and the metallic spring be thus permanentlv damaged 1 
(Fig. 62). 

Tables of Relative Values. 
To convert centimeters water into millimeters Hg. 

Cm. Mm. Cm. Mm. Cm. Mm. Cm. Mm. Cm. Mm. 

w. 11k. w. Hg. w. Hg. w. Hg. w. Hg. 

11 10 7 110 81 210 155 310 229 

2 1 20 15 120 89 220 162 320 236 

3 2 30 22 130 96 230 170 330 244 

4 3 40 30 140 103 240 177 340 251 

5 4 50 37 150 111 250 185 350 258 

6 4 60 44 160 118 260 192 360 266 

7 5 70 52 170 125 270 199 370 273 

8 <i 80 59 180 133 280 207 380 280 

9 7 90 66 190 140 290 214 390 288 
10 7 100 74 200 148 300 221 400 295 

To convert millimeters Hg. into centimeters water. 

Nm. Cm. Mm. Cm. Mm. Cm. Mm. Cm. 

Hg. w. 

210 285 

220 298 

230 312 

240 325 

250 339 

260 352 

270 366 

280 379 

290 393 

10 14 100 136 200 271 300 407 

The Potain instrument has never found favor in this country. 
It is generally and justly regarded as inaccurate, partly on account 
of its construction and largely on account of its application. Tt 
is still frequently used in France, however, with the idea of com- 
paring the pressure in different arteries — radial, temporal, dorsalis 

'v. Recklinghausen, II.: Neue A.pparat. /.. Messung dea arteriellen Blutdrucks 
beim Menschen, Munchen. med. Wehnachr., L913, l\i. 869. 



Hg. 


w. 


1 


1 


2 


3 


3 


4 


4 


5 


5 


7 





X 


7 


9 


s 


11 


'.! 


L2 



Hg. 


w. 


10 


14 


20 


27 


30 


41 


40 


54 


50 


68 


60 


81 


70 


95 


SO 


108 


90 


122 



Hg. 


w. 


110 


149 


120 


163 


130 


176 


140 


190 


150 


203 


160 


217 


170 


230 


180 


244 


190 


257 



ANEROID TNSTRl \i i:\rs L23 

pedis, etc. The pressure required to obliterate the pulse is applied 
directly over the artery, the compression being exerted upon the 
pelotte with the fingers. Thus it is verj easj to exert the pressure 
mainly against the tissues and bul slightly if at all upon t he artery. 

Francois Frank 1 has designed an instrument (sphygmopalpeur) 
for the transmission of arterial or venous pulsations without circular 
fixation, and recommends its use in connection with the Potain 
sphygmomanometer. It consists of a Marey tambour which is 
attached to an upright stand through a series of levels and joints 
so that it can be set at any angle or direel ion, the pressure exerted 
by it varied at will. Contrary to the usual findings, he obtained 
higher readings than with the Riva-Rocci instrument, a fad which 
he explains as follows: 

"The Potain apparatus acts only on the radial artery, while the 
method of circular compression by producing venous stasis reduced 
the amplitude of the arterial pulse and has the effed of counter- 
pressure, thus yielding too low a reading." 

The sphygmomanometer of Bouloumit consists of a combina- 
tion of the Potain and the Gartner apparatus. It has been used 
in an effort to study the relationship of arterial and capillary 
pressure. 2 

V. Subjective Method. — The subjective sensations of the patient 
may also be used to determine the systolic and diastolic readings. 
With the cuff and manometer applied in the usual manner the 
patient is told to notice the onset of throbbing in the arm below 
the cuff — this indicating the systolic pressure. The disappearance 
of the pulsatory sensations corresponds to the diastolic pressure. 
Quite accurate readings may thus be sometimes attained, but the 
procedure introduces a considerable and quite unnecessary amount 
of the personal equation, and is therefore rarely employed. 

Francois Frank 3 in contrasting the findings of the subjective 
method with those obtained by the Gartner instrument, found 
that the two phenomena (recoloration and sense of pulsation), 
although identical as regards the height of manometric pressure, 
are not so as regards time when compared to the beginning of the 
elevation of a volumetric curve, there being a temporal difference 
of from four to six seconds between the two. This emphasizes the 
importance of allowing pressure to fall slowly. He suggests that 

1 Compt. rend. Soc. de biol., 1909, lxviii, 525; Soc. biol., Paris, July 25, 190S, p. 226. 

2 Bouloumie's instrument described: Amblard: These de Paris, 1907, No. 261, 
p. 51. 

3 La sphygmomanometric digitale par le procede de Gaertner avec et sans anemie 
prealable, etc., Compt. rend. Soc. de biol., February 5, .1910, p. 234. 



124 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

the pulsatile phenomenon, which manifests itself later than the 
beginning of recoloration, indicates, when at its maximum, the 
in inimum pressure in the collateral arteries of the fingers; while 
the recoloration and the initial swelling is the index of the maximum 
pressure of the arterioles. He finds that the maximal digital arterial 
pressure is often approximately two-thirds that of the radial press- 
ure, although this relationship is by no means a constant one. 

Methods of estimating pressure based on subjective sensations 
are entirely too inaccurate to be of much use. This applies no less 
to recent refinements than to the method suggested by von Frey, 
which consisted in submersion of the arm in mercury and the meas- 
urement of its depth to the point at which the greatest pulsation 
was felt. 

Comparative Values. — The palpatory (lliva-Rocci) method yields 
results which are on the average 7.5 mm. Hg. higher for every 100 
mm. Hg. than the actual intra-arterial pressure, and 5 per cent. 
lower readings than are obtained by the graphic method, because 
a certain amount of arterial distention must occur before the pulse 
can be palpated. If a sphygmograph or a second (radial) cuff is 
used to determine the return of the pulse instead of the .finger, 
somewhat higher readings (10 to 15 mm.) will generally be obtained. 
The end of the maximum oscillation (diastolic pressure) can be 
more readily determined by this means than by palpation, especially 
in the case of the novice. 

The auscultatory procedure yields results which are closely com- 
parable to the graphic method, provided that the fourth phase 
(muffling) and the last of the large oscillations be chosen as the 
criteria of the diastolic pressure (Lang and Manswetowa, Bickel, 
Warfield, Schrumpf and Zabel, Engle and Allen). If the fifth 
phase is chosen Windle found that the results corresponded within 
5 mm. In the average case it will not make more than this degree 
of difference whether we choose the fourth or the fifth phase, but 
in cases with a long fourth phase the discrepancies may amount 
to 10 to 12 mm. With a little training the fourth phase is quite as 
readily recognized as the fifth. The vast majority of cases show 
readings o nun. higher by ausculatation than by palpation. 

The oscillatory (visual) method tends to yield higher values (5 
to 10 mm.) than that of palpation, and figures practically identical 
with the graphic method (Schrumpf and Zabel). It has a distinct 
field of utility in taking the pressures of infants and individuals 
with very small pulse-pressures. The greatest discrepancies occur 
in arteriosclerotic cases. 



1 VEROID INSTRUMENTS 125 

The graphic method is more time-consuming and troublesome 
than the other methods, bu1 in the hands of those who are familiar 
with its technic is the mosl exact. It is generally accepted as a 
standard of clinical accuracy. The actual readings are considerably 
higher than the endo-arteria] pressure. The margin of error maj 
be as high as 25 per cent. 

On close analysis Zabel found that when well-marked discrep- 
ancies existed between the findings of differenl methods, the phase 
of "large oscillations" was long, whereas in the class in which the 
results were closely in accord, this phase was brief. ( lareful observa- 
tion, he believes, shows that the phase of large oscillations really 
consists of two distinct parts. In the beginning the first large 
oscillations exhibit a crescendo quality which bespeaks the increas- 
ing pressure in the edges of the cuff. Following this in some cases a 




Fig. 64.— The diastolic pressure as determined by different methods. (Bickel.) 

second increase in the oscillation abruptly occurs, which corresponds 
to the Ehret phenomenon and to the beginning of Korotkow's 
third phase. According to this conception the first of these two 
diastolic phenomena occurs when the central portion of the arterial 
lumen is collapsed; the second, when the entire lumen is obliterated. 
Thus the 

First critical point = onset of large oscillations = beginning 
of fourth auscultatory phase = collapse of central arterial wall. 

Second critical point = onset of maximum oscillations = Ehret's 
phenomenon = third auscultatory phase = complete arterial 
occlusion. 

In corroboration of this hypothesis are the facts that (1) in 
brachial arteriosclerosis Ehret's phenomenon is of gradual, not 
sudden, onset; (2) lacks in its brusque quality, and (3) is some- 
times entirely absent. 



126 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 



RELATIVE ADVANTAGES OF THE DIFFERENT METHODS. 

In order to obtain the greatest accuracy (as in experimental 
work) and for the purpose of having permanent demonstrable 
records the graphic method excels. 

For routine clinical work where simplicity and celerity, com- 
bined with reasonable accuracy, are the chief desiderata, the auscul- 
tatory method is to be preferred. The older palpatory method offers 
more change for error, due to the personal equation, and with it 
much more difficulty is experienced in determining the diastolic 
pressure. Furthermore, the auscultatory method has to a con- 
siderable extent eliminated the question, "Which sphygmoman- 
ometer shall I buy?" Because with the last-name method any 
accurate manometer, if supplied with a suitable cuff, etc., will 
answer the purpose. 

The sphygmographic attachment at the wrist, aside from being 
troublesome to adjust, results in venous stasis, which elevates 
the curve and diminishes the excursions. The oscillatory devices 
have the disadvantage that the eye has to measure two different 
points at once. They are useful, however, when the pulse is small, 
and some of them can be used to register the pulsation in the smaller 
arteries. So far as clinical accuracy is concerned, it is not of great 
moment which method is employed. The results will generally 
not vary more than 10 mm. Hg., figures well within the range of 
allowable error. These clinical methods are after all only relative 
estimations, and if the same instrument is used on all cases, and 
the examiner is conversant with the technic, the results will be 
sufficiently accurate for comparison and for practical purposes 
generally. 

Sources of Error. — There is a more or less prevalent impression 
that marked errors in the clinical determination of blood-pressure 
may be brought about through the varying influence of the soft 
tissues surrounding the artery, such as the size and muscular 
development of the arm. 

In the investigations of Miiller and Blauel, 1 conducted on arms 
aboul to be amputated and controlled by manometrical pressure, 
readings from the artery directly showed that the broad cuff gave 
a reading about K) mm. higher than the actual pressure, a margin 
of error wliieh waxed larger as the width of the cuff was decreased. 

Zui Kritik des Riva-Roccischeii u. gartnerschen Sphygmomanometers, Deutsch. 
Arch. f. klin. Med., 1907, xci, 517. 



RELATIVE ID] INTAGES OF THE DIFFERENT METHODS L27 

But both EIi'iiscii 1 and Janeway- h;i \ c reported cases with very 
great differences between the sofl parts of the two arms atrophj 
flaccidity againsl hypertrophy i which yielded identical readings on 

the two sides. Certainly it' an error exists it lies well within the 
limits of d;iil\ physiological fluctuation, provided a cuff with a 
width of 12 cm. is employed. 

The extent of the role played by hypertonicity of the arterial wall 
in causing erroneous U l-pressure readings has been much dis- 
cussed. It has been claimed that some of the excessively high 
readings occasionally obtained in man (350 mm. or over) could 
not represent the actual endovascular tension, but musl be due 
to resistance of the arterial wall. 

The subject has been reviewed and studied in a series of 
ingenious experiments by Janeway and Park, 3 who found that 
although the arterial wall does offer definite resistance to com- 
pression, greater in large, thick-walled vessels, yet this resistance 
in a normal adult brachial is equivalent to only a few millimeters 
of mercury. In children it is an entirely negligible factor, and in 
adults with a normal blood-pressure the error thus introduced into 
clinical blood-pressure measurements is not greater than 10 mm. 
Hg., "a figure less than the spontaneous variations in pressure 
from minute to minute." 

"Atheroma, even of considerable degree, is without appreciable 
effect on the compressibility. Calcification of the arterial wall, 
when segments longer than 6 cm. are examined, increases only 
moderately its resistance to compression. The overpressure 
dependent on this factor in our experiments did not exceed 17 nun. 
Hg. In clinical blood-pressure determinations, if a wide arm-piece 
be used, and the return of the first fully developed pulse wave be 
taken as the index, as recommended by von Recklinghausen, even 
advanced arterial thickening and calcification probably do not 
introduce an error of any importance. The only factor altering 
the compressibility of an artery which seems capable of introducing 
an error of real importance in the clinical measurement of systolic 
blood-pressure is the state of contraction of the arterial walls. 
It is impossible from our experiments on surviving ox arteries to 
set definite numerical limits for this in man. From these experi- 

!Beit. z. Physiol, u. Path. d. Blutdrucks, Deutsch. Arch. f. klin. Med., 1900, 
Ixviii, 443. 

2 Influence of the Soft Tissues of the Arm on Clinical Blood-pressure Determina- 
tions, Arch. Int. Med., 1907. 

3 An Experimental Study of the Resistance to Compression of the Arterial Wall, 
Arch. Int. Med., November, 1910. 



128 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

mentSj however, combined with our study of human arteries after 
amputation and postmortem, we feel that a degree of hypertonic 
contraction of the brachial artery sufficient to cause an error of 
more than 30 mm. Hg. seems improbable, and of more than 60 mm. 
incredible, during life" (Janeway). 

Practically all the evidence at hand supports the foregoing 
statements. The latest corroboration is furnished by Macwilliam 
;iiid ECeeson, 5 who found that relaxed arteries (Ringer's solution, 
manipulation, sodium fluoride) with normal or thickened walls 
yielded only trivial degrees of resistance to compression. Thickened 
arteries from old animals, especially when contracted (barium 
chloride, epinephrin) below the body temperature, were capable of 
exerting considerable resistance. In the smaller arteries constric- 
tion was sometimes sufficient to resist a passage of fluid of 440 
mm. Hg. Arterial contraction in such arteries could be greatly 
diminished by repeated or long-continued compression and by 
massage of the artery. This procedure, they suggest, may be used 
to determine how great a percentage of a high pressure is due to 
vascular resistance, although it does not enable one to determine 
whether this vascular resistance is due to arterial contraction or 
to other causes. 

They have further shown that soft spots in the course of an 
irregularly sclerosed artery are not bridged over by the brachial 
cuff but that the latter acts effectively even in very limited soft 
areas, thus preventing the resistance offered by the reet of the 
artery from having any great effect upon the readings of the 
instrument. 

Much stress has been laid by some investigators upon variability 
of the cond action of the pulse wave due to alteration in the arterial 
lumen and changes in the resiliency of the arterial wall. Thus 
Hill believes that systolic pressure readings are affected by (a) 
the actual maximum pressure of cardiac systole; (b) the conduction 
( >!' t he pressure wave to the periphery. The resistance of the arterial 
wall to compression affects the systolic index of blood-pressure 
but little, but the relative hardness or softness of the vessel affects 
the conduction of the systolic wave considerably, especially if 
it is large. The force of the wave is damped down in soft arteries 
as sound waxes are damped by velvet. 2 

l The Estimation of Systolic Blood-pressure in Man, with Special Reference to 
the Influence of the Arterial Wall, Heart, L913, iv, 279. 

-Hill, L.: Measurement of Systolic Blood-pressure in Man, Heart, 1910, i, 73. 
Hill and Rowlands: Heart, 1912, iii, 219. 



PRECAUTIONS To HE oUSERVED IN TAKING READINGS 12!) 

Most of the experimental evidence, however, indicates that 
constrictions of the artery snllicicnt to cause any considerable 
diminution of conduction can hardly occur between such large 
vessels as the aorta and brachial artery; and further, t hat increased 
arterial rigidity is equally insufficient to cause an important source 
of error. The difference in pressure obtained in arm and leg, or two 
arms or two legs, is the result of pressure differences in the arteries 
in question, and not due to abnormal conduction of the aortic 
pressure. 

The elasticity of the aorta and its branches is important in 
causing a lower systolic and a higher diastolic pressure in the 
systemic arteries than would a rigid tube, but in blood-pressure 
estimations by the obliteration method, the resiliency of the inter- 
vening arterial tube appears to be negligible. 1 

PRECAUTIONS TO BE OBSERVED IN TAKING READINGS. 

Blood-pressure readings should, for purposes of comparison, 
always be taken in the same (preferably the horizontal) posture. 
At all events the position should be such that the reading is made 
at a point about on a level with the heart, thus eliminating the 
error due to the weight of the blood column. When possible, 
observations should be made about the same time of day and in 
the same relation to meals. They should not be taken during 
excitement, after exercise, or shortly after the patient has partaken 
of hot food or drink, tea, coffee or alcohol, and not when the extremi- 
ties are overheated or chilled. All muscular activity on the part 
of the patient must be prevented and complete relaxation, both 
general and local, obtained. Observations made under conditions 
of spasm — subsultus, tetanus, etc. — are absolutely unreliable. 
Edema of the tissues is also a fertile source of error, and readings 
obtained from anasarcous patients are of no value. Fear, excite- 
ment or psychic effort have a marked effect on the blood-pressure. 
In taking one's own pressure, higher results are often found than 
those obtained by another observer immediately before or after- 
ward, simply as the result of psychic concentration. Schrumpf 
relates an instance in which the anticipation of an austere prognosis 
raised the pressure of a patient 33 per cent., to fall again promptly 
when reassurance was forthcoming, and only to rise once more 
when complaining of his insomnia and worries. Gibson found that 

1 Macwilliam, Kesson, and Meloin: The Conduction of the Pulse-wave and its 
Relation to the Estimation of Systolic Blood-pressure, Heart, 1913, iv, 393. 



130 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

his own pressure was increased 35-40 mm. after delivering a lecture. 
Due allowance for variability of the systolic pressure must always 
be made in m urotic patients. 

Von Recklinghausen observed in his own case a rise of 14 cm. 
H 2 caused by the entrance into his presence of a person whom he 
intended t<> berate (see Physiological Variations). Putermann 1 
found that the anticipation of an examination almost without 
exception raised both blood-pressure and pulse rate in school- 
children. In extreme cases psychic states may cause a rise of 90 
nnn. Hg., generally in association with marked pleasure, anger, or 
fright. The diastolic pressure in these cases is practically unaffected. 9 
The interposition of a thin undergarment between the cuff and 
the arm is unobjectionable, in fact, may be positively beneficial. 
In cold weather a chilly cuff applied to the arm, both by the dis- 
pleasure it causes the patient, and by the stimulating effect it has 
upon the vasomotor nerves, may yield erroneous readings. In 
very high-strung individuals it is best to warm the cuff before 
applying it. 

It sometimes happens that the initial systolic blood-pressure 
reading on a given subject yields distinctly higher figures than can 
be obtained in subsequent attempts. Gallavardin and Haour 3 
found, in the study of 100 cases, that this initial high pressure, 
which may amount to 35 mm. in women and 25 mm. in men, may 
last fifteen minutes, although in 50 per cent, of these cases the 
normal point was reached at the end of five minutes. Only the 
systolic pressure was affected, the diastolic level remaining constant. 
These figures are certainly high. 

Such an increased pressure may be due to: (1) Psychic influences 
— excitement or fear, chiefly noted in high-strung individuals. 
(2) Pain- arising from the forcible inflation of the cuff on sensitive 
arms or in cases of marked hypertension. (3) Local stimulation 
of the vasomotor nerves from pressure. (4) Prolonged application 
of the cuff. This tends to relax the artery, and by reflexly dimin- 
ishing the force of systole, possibly lessens the conduction of the 
pulse wave. It also produces marked increase in the venous pressure 
and congestion of the tissues below the cuff. 

Attention has been called to the fact that in estimating the 

Ueber <1. Beeinflussung d. ZirkulationsBystem durch d. Schulezamlna, Wien. 
med. Wchnschr., I'.tni, liv, 265. 

'Schrumpf, P.: Die psychogene Labilital des Blutdrucka u. ihre Bedeutung in 
<!. Praxis, Deutsch. med. Wchnschr., L910, xxxvi, 2385. 

Braise Bystolique de la tension arterielle au moment de la mensuration, Arch, de 
mal. 'In ccsur, etc., 1912, \ , si. 



THE PERSONAL EQUATION OF THE EXAMINER L31 

diastolic pressure b\ increasing tbe manometer pressure, differenl 
results arc sometimes obtained than when the diastolic index is 
taken during a falling manometric pressure, especiallj if the press- 
ures are gauged <>n both arms simultaneously. A comparison of 
the diastolic values with a rising pressure may thus indicate au 
abnormal tendency toward blood-pressure variatioE in a given 
individual. 1 



THE PERSONAL EQUATION OF THE EXAMINER. 

Schultze 2 found that ordinarily with a trained observer a series 
of ten successive measurements will yield a fair average of accuracy. 
Much closer correspondence in successive readings is obtained if 
the manometer is read and the pulse palpated by the same person, 
than if these duties are relegated to two individuals. This results 
from the strained mental attitude of the palpator who is almost 
certain to become "the dupe of expectant attention,'' knowing 
that his sense of touch is being "controlled" and fearing lest, after 
all, he fail to feel the first pulse wave. His sense of perception being 
therefore raised to its maximum, it often happens that he becomes 
subjectively conscious in his finger-tips of his own pulse, especially 
if, as is necessary for accuracy, the manometric pressure is allowed 
to fall but slowly, and the procedure is therefore prolonged. Sub- 
jective appreciation of the pulse is more marked in the second 
finger, and in certain individuals. It is generally perceived from 
ten to thirty seconds after the finger-tips of a dependent hand have 
been lightly placed upon a solid object (e. g., table). This factor 
is in our experience only rarely a cause of confusion. 

The frequency with which the subjective pulse appears in "con- 
trolled" observers indicates how variable is the acuteness of our 
tactile perception. If the pressure is read and the pulse is palpated 
by the same individual the discrepancies of successive readings 
will be far smaller, owing to the subjective suggestible element 
(expectant attention). The first reading having yielded a definite 
result, we consciously or unconsciously "expect" the pulse to 
reappear at about the same level. This is illustrated by Schultze 
in Fig. 65, which shows how much more closely the results of ten 

1 Macwilliam, J. A., and Melvin, G. S.: The Significance of Blood-pressure 
Readings in Man, British Med. Jour., 1914, p. 777. 

2 Ueber d. psychologischen Fehlerquellen bei d. palpatorischen Bludruckmes- 
sung nach Riva-Rocci u. v. Recklinghausen: Arch. f. d. ges Physiol., Bonn, 1908, 
exxiv, 392. 



132 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

consecutive readings corresponded when the suggestible element 
is not eliminated. 

In the first two estimations, I and II (10 each), the examiner 
observed the manometer while feeling for the pulse wave; in the 
last two, III and IV, the manometer was not read until after the 
pulse wave was perceived. 1 When the suggestible element was 
eliminated, successive readings tallied less closely. 



150 




HO 


I 












130 


11 \ 






















150 








r 


\ 




UO 


III 


^\ 


r 


/ 


v 


/ 


430 




\ 


( 




V, 


















HO 














130 


IV 





























Fig. 65. — In the first two estimations, / and //, the manometer was observed while 
feeling the pulse wave. In the last two, III and IV, the manometer was not read 
until after the pulse wave had been perceived. 



Another possible source of error lies in the fact that the threshold 
of perception for the appearing and disappearing pulse are not the 
same. In the former we judge of a subsensible stimulus which 
is being raised to, in the latter of a sensible stimulus which is being 
lowered beyond, the point of perception. The point of disappear- 
ance is definitely more difficult to determine. Finally, the mercury 
in the manometer rarely if ever rises or falls so gradually that the 
examiner lias lime to decide for each individual millimeter of 
pressure whether or not a pulsation is present. Therefore our 

'Schultze: CJeber d. psychologiachen Fehlerquellen dei d. palpatorischen Blu- 
druckmessung oach Riva-Rocci u. v. Recklinghausen: Arch. f. d. Res Physiol., 
Bonn, 1908, exxiv, 392. 



ACCURACY AND SIGNIFICANCE OF BLOOD-PRESSURE 133 

measurements are for subjective reasons generally exact only within 
3 or 5 mm. Hg. 

In order to minimize all these sources of error the following pro- 
cedures should be adopted: (1) Discard the result of the first 
reading, using it simply to demonstrate the harmless and painless 
character of the procedure; and when possible make subsequent 
readings after some little time has elapsed. (2) Avoid making 
blood-pressure estimations when the subjecl is excited, anxious or 
worried, as a result of the examination, etc. (3) Make several 
consecutive readings and if they correspond more or less closely, 
take the arithmetic mean. ( I) Make the observations as quickly 
as is consistent with accuracy; do not look at the manometer until 
the pulse is felt — at this point the air escapemenl should he tightly 
closed until the reading is made. (5) Allow the pressure to fall to 
zero between observations, and permit sufficient time to elapse 
between readings for the venous pressure (stasis) to fall to the 
normal level. Never make a reading with a broken mercurial 
column, and be sure that the mercury corresponds with the zero 
on the scale before inflation. Needless to saj . most of these sources 
of error are eliminated by using the auscultatory method which 
has therefore come into merited favor. 

In certain forms of cardiac arrhythmia, especially auricular fibrilla- 
tion and extrasystole, it becomes very difEcuh to gauge the blood- 
pressure, as the pulse is never equal in volume or in tension for 
many consecutive beats. A rough estimate of the actual pressure 
may be obtained by measuring first the strongest and then the 
weakest pulsations and thus establishing an average. (See Auricular 
Fibrillation.) 

Possible Accidents. — In certain dyscrasic states — purpura, hemo- 
philia, etc. — too prolonged application of a highly inflated cuff 
may cause capillary hemorrhage. This is very rarely the case. 

Mohr has reported thrombosis following repeated blood-pressure 
observations in a patient suffering from tuberculous pneumonia. 
This is, we believe, the only case of the kind on record. Hill has 
reported edema in a paralytic arm following the application of the 
cuff in a case with a blood-pressure of 220 mm. 

THE VALUE, ACCURACY AND SIGNIFICANCE OF BLOOD- 
PRESSURE ESTIMATIONS. 

Blood-pressure readings furnish us with important and valuable 
data, but they must be interpreted in relation to other physical 



134 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

signs. Such observations alone do not furnish us with a basis for 
treatment any more than they, unaided, permit us to make a diag- 
nosis. In this respect a sphygmomanometer is like a thermometer 
— its readings must be construed in the light of other findings. 
We have seen cases exhibiting a practically normal systolic and 
diastolic pressure associated with dyspnea, cyanosis, and edema, 
showing that the blood flow was not normal. 

Observations of the systolic pressure alone are of relatively little 
value. They indicate, it is true, the strain to which the arteries 
are subjected, but the diastolic pressure, the variations of which 
correspond more or less closely to those of the mean pressure, is 
the real indication of the work the heart has to do. Systolic pressure 
may suddenly vary greatly from many diverse causes — fright, 
excitement, etc. — but the diastolic pressure is a much less easily 
disturbed factor, and may hence be a valuable criterion in deciding 
whether organic, vascular or cardiac changes are present. Since 
the diastolic pressure can now be readily, quickly and accurately 
determined by observing the appearance of the fourth auscultatory 
phase, there can no longer be any excuse for neglecting this far more 
important of the two phases of arterial tension. We have already 
learned in most conditions to attribute more importance to the 
diastolic than to systolic readings. 

Pulse-pressure. — The difference between the systolic and the 
diastolic pressure roughly indicates the volume of the pulse. From 
a study of pulse-pressure certain deductions can often be drawn, 
but it must be remembered that these are not absolute nor always 
trustworthy criteria. 1 

Systolic Diastolic Pulse- 

pressure, pressure. pressure. 

increased peripheral resistance . . + ++ — 

Decreased peripheral resistance . . — + 

Increased heart rate + + + — 

Decreased bearl rate — + 

Increased systolic discharge ++ + + 

Decreased systolic discharge ... — — 

The diastolic pressure is normally about three-fourths of the 
systolic pressure and the pulse-pressure, one-quarter of the systolic 
pressure. A pulse-pressure persistently as low as 20 or as high as 
60 nun. is definitely pathological. 

The norma] pulse-pressure in adults ranges between 30 and 
50 nun. A pulse-pressure of 45 approximates the average normal 
for individuals below the middle period of life. 

1 Wiggere, C. J.: Modern Aspects of Che Circulation in Health and Disease, 
Philadelphia, 1915, p. 68. 



ACCURACY AND SIGNIFICANCE OF BLOOD-PRESSURE 135 

As long as the aorta is clastic and the arteries resilient this amount 
of increased pressure is sufficient to keep up an adequate peripheral 
blood How. When, however, the vessels become sclerotic, a larger 
systolic output is required to maintain peripheral nutrition and hence 
the pulse-pressure must be increased. This increase which is met 
with after the middle period of life is therefore a compen ator 
phenomenon, which within certain limit- ma\ be regarded as an 
index of the degree of sclerosis present. 

The normal pulse-pressure increment is greater after sixty years 
than between forty and sixty. 

As a method of calculating what the norma] for a given individual 
should be, Oliver suggested the following rule: Add to the average 
pulse-pressure before forty (I. e., 45 nun.) 1 mm. foreverj two years 
from forty and sixty years and 1 mm. per year for each year after 
sixty. Thus a man of seventy years would be entitled to a pulse- 
pressure of 65 mm. (/. e., 45 -f- 20). 

The increased pressure of advancing years results from cardiac 
hypertrophy and when merely normal aging, is due mainly to an 
increase of the systolic pressure. If an increased pulse-pressur< 
once established, subsequently diminishes, a- the result of a rising 
diastolic pressure, we are warranted in assuming that a pathological 
factor has been added. In other words, we are no longer dealing 
with a normal senile change, but with an abnormal vascular con- 
dition; generally B right's disease. 

A large pulse-pressure if constantly maintained will be found 
associated by left ventricular enlargement and myocardial hyper- 
trophy. In addition, dilatation of the aortic arch is also generally 
encountered. Warfield 1 states that when the pulse-pressure exceeds 
70 mm., the large distributing arteries will be found enlarged, and 
upon microscopic examination will show fibrosis of the medial coat. 

Large pulse-pressure is encountered: in aortic insufficiency, 
chronic nephritis, arteriosclerosis and in exophthalmic goitre, and 
in many vasomotor crises. Small pulse-pressures are met with in 
asthenic conditions, when the muscle is no longer able to supply 
the required systolic output. This is often seen in failing compen- 
sation, in mitral and aortic obstruction, in shock, collapse, anemia, 
hemorrhage and cachexia. Pulse-pressures of less than 30 mm. are 
not often encountered over prolonged periods because the blood 
supply is apparently insufficient to maintain the f unctionation of the 



The Significance of High Pulse-pressure, Jour. Am. Med. Assn., 1917, lxviii, S24. 



136 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

As a rule the rate of blood flow through the arterioles tends to 
vary (within certain limits) directly with the pulse-pressure. 1 The 
functional efficiency of the viscera, as shown by perfusion experi- 
ments, also stands in a direct relation with the size of the pulse- 
pressure. In order that secretion and excretion shall occur there 
must exist not only a given pressure but an intermittent pressure. 
The flow of urine as well as its urea and chloride content, varies 
directly with the pulse-pressure 2 and the diuresis of digitalis and 
strophanthus is due to the increased pulse-pressure which these 
drugs produce. 3 The importance of the pulse, and the diastolic 
pressures far exceeds in value the estimation of the systolic pressure 
alone. 

A high systolic, with a normal diastolic, pressure may result from 
emotional disturbances and as a result of physical exertion. 

.1 low systolic, with a high diastolic, pressure often indicates myo- 
cardial weakness in association with severe pressor factors such as 
nephritis or vascular spasm. 

A low systolic and diastolic pressure occurring in a person who 
is up and about (essential hypotension) , while it does not necessarily 
imply a poor circulation, is definitely associated with diminished 
reserve force — "staying power." 

A high systoKc, with a low diastolic, pressure is most characteris- 
tically seen in aortic insufficiency; it may, however, result from 
peripheral vascular dilatation associated with forcible heart action. 

THE EXTREMES OF PRESSURE COMPATIBLE WITH LIFE. 

Hypertension. — Systolic blood-pressures above 235 mm. are 
unusual and above 250 mm. are rare. Hirst has reported a recovery 
in puerperal eclampsia with a pressure of 420 mm. Ilg. Needless 
to say, such a pressure could not long be maintained without some- 
thing giving out. Many patients live for years with pressures 
ranging about 200 systolic and 120 diastolic, and occasionally such 
pressures are compatible with hard manual labor, 4 but a sudden 
t en 1 1 iiiation in these cases is always a possibility. Strauss's patient 
lived for five years with a systolic pressure between 260 and 270 mm. 
( look and Briggs reported 400 mm. in a case of cerebral hemorrhage. 

1 Macwiltiam, .1. A., and Melvin, G. S.: British Med. Jour., 1914, i, 693. 
Erlanger and Honker: Johns Hopkins Hosp. Rep., 1904, xii, 346. Hooker: 
Arch, Ini. Med., L910, v, 491. 

I \in. Jour. Physiol., L913, xxxii, 70. 
*McCurdy, S. M.: Physical Examination and Regeneration of Kmployees, Jour. 
Am. Med. Assn., L915, Ixv, 2050. 



CHOICE OF AN INSTRUMENT 137 

Hypotension. A systolic pressure of 105 is common among many 
essential hypotension cases which are up and about. Not many 
are able to be so, however, if the systolic pressure falls below LOO 
or the diastolic below 50. Rolleston has reported a remarkable 
case of a man with a lingua] carcinoma, who lived for several weeks 
with systolic and diastolic pressures of 70 and 35 respectively. 
Agonal systolic pressures of 40 mm. have been reported and 60 
mm. probably represents the lowesl figure at which the coronary 
and medullary circulation can be kept up, even for a short time. 
Some of the earlier figures, such as those of John, of 35 to 40 in 
a case of advanced tuberculosis, are open to question on account 
of faulty instrumentation. Janeway has seen systolic pressures of 
40 mm. as transient phenomena during surgical operations. 

All clinical blood-pressure estimations must be accepted only as 
approximately correct. In addition to the fact that the determi- 
nation of the diastolic pressure presents certain difficulties we are 
confronted with the fact that, even if this could be accurately 
measured, we would still be only measuring the blood-pressure <>\' 
the brachial artery. Living vessels possess a distinct tonus — the 
ability to contract and to dilate — the amount of which in a given 
case we are thus far unable to determine. In addition to this 
we must bear in mind that the blood-pressure mechanism is an 
extremely labile one which is subjeel to frequent fluctuations, due 
to many different causes. 

On the other hand, thousands of blood-pressure measurements 
on different individuals have shown that pressure relations are 
fairly constant under similar circumstances; that there are definite 
and distinct bounds beyond which normal variations do not extend, 
and again that there are certain abnormal values which, if con- 
stantly found in a given individual, point very definitely to well- 
established pathological conditions. 

THE CHOICE OF AN INSTRUMENT. 

For general office work some instrument of the Riva-Rocci type 
is unquestionably to be preferred. Of this type of instrument a 
great many different models have been placed on the market. 
Although varying in detail of construction they are all based on 
the same principle. Good results may be obtained with most of 
them. On the whole, the last model of Nicholson's sphygmo- 
manometer is the most satisfactory instrument to be obtained, 
being compact, readily portable and yet possessing the advantages 



138 INSTRUMENTAL ESTIMATION OF BLOOD-PRESSURE 

of the mercury monometer. The "Baumanometer," although 
more bulky and less readily portable, is supplied with a very large, 
clear scale which is individually standardized. 

In the personal choice of an instrument we should be governed 
by a number of factors, i. e.\ (1) Accurate standardization. (2) 
General workmanship. The instrument should be made of flint 
glass, as the lead in American glass reacts with the mercury. In 
the same way the mercury will form an alloy if allowed to come in 
contact with any metals save steel and platinum, producing tur- 
bidity and increasing friction. It is also affected by rubber, owing 
to the sulphur which this substance contains. All joints must of 
course be tight. It is essential for accuracy that the cuff have a 
width of 12 cm. and that the canvas or leather backing be suffi- 
ciently rigid to maintain the width of the aforesaid rubber portion. 
(3) Compactness and portability — including the ease and celerity 
with which the instrument can be set up for use, the devices 
employed to prevent the spilling of the mercury when in transit, 
and the bulk of the apparatus when taken down. (4) The ampli- 
tude of the pulsation transmitted to the mercurial column. If the 
auscultatory method of blood-pressure reading be employed, the 
amount of visual oscillation obtainable loses its importance, and 
siti^factory results may be obtained with any accurate manometer 
if fitted with a proper cuff. 

Compres8edr-air manometers are small and accurate (since the 
stopcock when open equalizes barometric and temperature varia- 
tions). The adjustment of the drop used as an indicator is some- 
times troublesome. Aneroid instruments for bedside use, owing 
to their small size and ready transportability, have much to com- 
mend them. When well made they may not require adjustment 
for considerable intervals, although comparisons with a mercury 
manometer must from time to time be made. 

Spring manometers require frequent standardization, without 
which procedure inaccuracies may result. The von Recklinghausen 
apparatus is somewhat bulky and is based on cubic centimeter H 2 0, 
which standard has not been widely adopted. 

The kind of pump selected is of minor importance. The rubber 
bulb is light but less durable than the heavier metal variety. The 
von Recklinghausen bicycle-pump type is both heavy and bulky, 
but one or two strokes suffice for inflation. Compressed-air tanks, 
Mich as are currently used in rhinological work, may be used when 
rapid inflation of the cuff is desired. Errors due to stasis may thus 
be minimized. 



CI [SSIFICATH>\ <>F i;l.(H)I)I'h'h;SSUJiE I.XSThT )f 1-XTS 130 

CLASSIFICATION OF BLOOD-PRESSURE INSTRUMENTS. 

I. Mercurj i nanometers: 

1. Reservoir: Riva-Rocci, Cook Stanton, Nicholson, 

Hill, Kercher, Hollman, Gartner, Westenrijk, 

2. U-shaped: Baum, Janeway, Faught, Martin, Linnell, 

Fellner, Hamilton, Schneider, Beachler, Brown. 

II. Compressed-air manometers : Oliver, Bendick, Herz. 
III. Aneroid manometers: Sanborn, Rogers, Brunton, Tycos, 
Faught, Pachon, Jacquet, McKesson, Bristol, Fag. 

I\'. Spring manometers: von Recklinghausen. 

Y. Instruments for graphic registration: Krlanger, Gibson, 
Bingel, Singer, Uskoff, Silbermann, Brugsch, Stni-sberg, 
Muenzer, Strauss-Fleischer, Bussenius, Wybauw. 

VI. Instruments consisting of or which may he fitted with special 
oscillating indices, such as the Kcdde or Pal oscillom- 
eters, Bing, Nicholson, Vaquez, Faught, Widmer. 



CHAPTER IV. 
VENOUS BLOOD-PRESSURE. 

By J. HAROLD AUSTIN, M.U. 

Various methods of (determining venous blood-pressure in man 
have been devised. They may be grouped into five types: 

I. Gartner's Phenomenon. — Gartner, 1 in 1902, contended that if 
the left arm he slowly raised, the veins at the elbow which become 
distended when the arm is dependent will suddenly collapse upon 
reaching a certain level. He assumed that the elevation of this point 
above the level of the right auricle is a measure in centimeters of 
blood of the pressure at the right auricle. It is to be remembered 
that 10 cm. of blood equals 10.0 em. of water. As the level of the 
heart Gartner took the junction of the upper border of the left fifth 
costal cartilage with the sternum. Oliver 2 used the same method 
but observed the veins on the dorsum of the hand. Prym, 3 however, 
showed that Gartner's phenomenon occurs at different levels when 
the arm is raised at different rates, and that, moreover, the veins 
have a tonus of their own which may be stimulated by cold or 
by stroking, and this tends to accelerate their collapse. Meinertz- 
has noted that exercise of one arm frequently raises the level at 
which the veins collapse in that arm without affecting the level 
in the other arm. The state of the circulation and vascular tonus 
locally, as well as the pressure in the right auricle, therefore influence 
Gartner's phenomenon. 

II. Spring Manometers. In 1898 Oliver 6 attempted to measure 
venous pressure by means of a spring-pressure manometer. A 
button attached to the spring of the manometer was pressed against 
one of the larger veins of the arm with sufficient force to obstruct 
the How. The vein for an inch or so proximal to this point was 
then stripped by the finger. The pressure against the vein by the 
manometer was then gradually reduced and at the moment the 

1 Munchen. med. Wchnschr., 1904, badv, 2038. 

2 Quart. Jour. Med., Oxford, 1907-08, i, 59. 
• Mtinchen. med. Wchnschr., L904, li, 60. 
«ZtBchr. f. exper. Pathol, u. Therap., L908. 

i Jour, Physiol., 1898, xxii, li; 1898, xxiii, v. 



PRESSl RE <ll I MBER& 01 ER THE I El \ 



111 



emptied section of vein began to fill, the pressure recorded by the 
manometer was noted. This was believed to equal the venous 
pressure at that point. Subsequently both Frey 1 and Sewall 2 
independently devised similar spring manometers. 




Fig. 60. — Hooker's venous pressure apparatus. A small glass chamber i B) measur- 
ing 1 by 2 cm. is held temporarily by a rubber band over a suitable vein <m the back 
of the hand, as shown at A. A rim of collodion is applied and in drying it seals 
the chamber to the skin. The rubber band is then removed and the chamber con- 
nected by a rubber tube to the water manometer (M). By pressing on the man- 
ometer bulb (C) the air-pressure in the chamber is raised and a reading is made "at 
the point where slight oscillations of pressure cause the vein shadow to come and go 
promptly just before the vessel is completely collapsed." This pressure is recorded 
directly by the water manometer. The hand is held at the level of the midpoint of 
the anteroposterior diameter of the body at the costal angle. 

HI. Pressure Chambers Over the Vein (Fig. 66). — In 1904 von 
Basch 3 attempted to measure venous pressure by placing a small 
glass cylinder over the vein, and raising the air-pressure in the 



1 Deutsch. Arch. f. klin. Med., 1902, lxxiii, 511. 

2 Jour. Am. Med. Assn., 1900, xlvii, 1279; Tr. Assn. Am. Phys., Philadelphia, 
1900, xxi, 20. 

3 Wien. klin. Rundschau, 1900, pp. 549 and 572. 



142 VENOUS BLOOD-PRESSURE 

cylinder until the vein collapsed or releasing the air until the vein 
refilled. This method was improved upon by von Recklinghausen, 1 
and later by Hooker and Eyster, 2 so as to reduce the error caused 
by pressure of the wall of the cylinder against the vein. The latter 
authors compared readings made with a manometer in the facial 
vein of a dog with those made with their instrument over the neigh- 
boring exposed external jugular. The pressure was artificially 
altered by tilting the animal's body. The results follow: 

fflano&eter in Pressure chamber over 

Observation. facial vein. external jugujar. 

1 4.5 cm. H2O 4 cm. H2O 

2 10.0 cm. H 2 10 cm. HsO 

3 13.0 cm. H2O 14 cm. H2O 

4 5.0 cm. H2O 5 cm. H2O 

A further improvement of this instrument has been made by 
Hooker, 3 and in its present form the instrument has proved most 
satisfactory. Two conditions are necessary for its use : First, that 
the vein shall stand out sufficiently from the surrounding skin 
level to give a distinct shadow by oblique illumination, and, second, 
that the vein wall must be collapsible. Hence "old patients with 
phlebosclerosis, patients with exceedingly edematous or fat hands, 
and patients with continuously small veins are not satisfactory 
for this method" (Clark). 

IV. Double-cuff Manometers (Fig. 67). — In 1912 two instruments 
upon the same principle were introduced independently, one by 
L. Frank and M. Reh 4 and the other by A. A. Howell. 5 The instru- 
ments consist of two cuffs, each attached to a water manometer. 
One cuff is applied to the upper arm, the other to the forearm. 
The forearm cuff is inflated so as to fit against the arm snugly 
without exerting, however, more than 1 cm. (Frank and Reh) to 
3 cm. (Howell) H 2 pressure. The upper cuff is then slowly inflated 
until 1 he water in the forearm manometer is seen to be rising. This 
rise is assumed to be evidence that the venous flow beneath the 
upper cuff has been obstructed and that the blood, being dammed 
back, has increased the volume of the forearm with consequent 
displacemenl of air from the lower cuff and a rise of water in its 
attached manometer. The forearm cuff and its manometer are 
used, therefore, as a sort of plethysmograph. It is further assumed 
that the blood flow beneath the upper cuff is first obstructed when 

1 Arch. f. exper. Path, u, Pharm., L906, Iv, 163. 
•Johns Hopkins Boap. Hull., L908, \ix, 274. 

\m. Jour. Physiol., I'.U I, xxxv, 73. 
< Ztschr. 1. exper. Path. u. Therap., Berlin, L912, x, I'll. 

Arch. Int. Med., L912, ix,'l is. 



INTRA \ ENOl S NEEDLE 



143 



the pressure in this cuff equals the venous pressure. The instrument 
of Frank and Reh differs from Howell in that i1 provides For graphic 
registration of the readings. Reference to the table on p. 146 
shows that Howell's figures are somewhat higher than those of 
Frank and Reh, which may be in pari explained l>\ the higher 
pressure used by Howell in his plethysmography cuff. 



D l 




Fig. 67. — Howell's venous pressure apparatus. Upper and lower cuffs applied 
and attached to their respective water columns. E. lighl cuff for constricting upper 
arm and obstructing venous return; F, glass T and bulb, by means of which pressure 
is raised in E; G, water column measuring pressure in E; B, inelastic covering of 
light material encircling rubber bag; C, glass T, side tube, and clip, by means of which 
pressure can be raised; D, water column measuring pressure. 



V. Intravenous Needle. — In 1909-10 Moritz and von Tabora 1 
published studies of venous pressure measured by the pressure 
required to cause normal saline to enter the median vein at the level 
of the heart. The method was to place the patient in the recumbent 
position, and then introduce into the median vein with the usual 
precautions a needle connected with a burette of normal saline. 
The saline was allowed to enter the vein, its level in the burette 
falling until further flow ceased. The level of the saline above the 
heart was then read, and the resulting figure was assumed to be the 
venous pressure at the heart in centimeters normal saline, which 
since 10 cm. normal saline equals 10.07 cm. H 2 may be reckoned 
as cm. H 2 0. In all the other methods described the patient is 

1 Deutsch. Arch, f; klin. Med., 1909-10, xcviii, 475. 



144 



l " EN OUS BLOC) D-PRESS UR E 



in sitting posture, and the level of the heart is by most observers 
taken according to von Recklinghausen's rule as at the level of 
the apex of the subcostal angle. With the patient recumbent 
Moritz and von Tabora assume the heart level to be that of a 
point <>n the fourth rib 5 cm. below the level of the anterior thoracic 
surface. This method of measuring venous pressure is the most 
accurah of those described for use in m<iu. 




Fig. (is. The Moritz-Tabora venoua blood-pressure apparatus: .1, cannula 
B, manometer scale; C, level; I), escapement. (After Hoffmann.) 



Capillary Pressure. — In 1875 the attempt to measure capillary 
pressure was first made by VOD Kries. 1 A small glass plate of 
known area was laid upon the skin or mucous membrane and 
pressure was exerted evenly upon it by means of delicate weights. 

1 Berichte u. d. Verhandlung der koniglich sachsisch, < lesellschaft d. Wissen- 
schaften /.. Leipsic ninth. Phys., is?."., .'lxwii, 147. 



CAPILLARY PRESSl RE 1 i;, 

The amount of weight required to produce a just perceptible 
pallor of the skin or mucous membrane was taken to be the capillar} 
pressure, and the weigh.1 and area over which ii acini being known, 
the pressure per unit of area and hence the pressure in millimeter 
Hg. (1 mm. II»'. = 0.0136 gm. per square millimeter) or in centi- 
meter IIjO (1 cm. IU) = 0.01 gm. per square millimeter) can be 
calculated. VonBasch and von Recklinghausen measured capillary 
pressure with the same apparatus employed for measuring venous 
pressure by applying it overa skin area, the former noting the press- 
ure required to just cause complete blanching, the latter raising 
the pressure above the point required to produce complete pallor, 
and on gradually lowering the pressure noting the momenl when 
flushing first became apparent and also when Hushing became 
complete. 

Lombard 1 has recently developed a refinement of these methods. 
He finds that if the skin be wet with glycerin or with a transparent 
oil, by the use of a low-power magnification (from 10 to 35 
diameters), and either bright daylight or a Nernsl lamp, I tie papilla' 
of the skin with their superficial bloodvessels are rendered visible. 
He applies this method either with a weighted glass plate according 
to von Kries, or with a specially constructed chamber similar in 
general principle to von Recklinghausen's. Lombard's chamber 
consists of an inverted truncated cone. The smaller end, which 
fits against the skin, has a diameter of 2-4 mm., its walls are 3 nun. 
thick, and the pressure is therefore applied over a circular area 
of 18 mm. in diameter. Over the periphery of this area the skin is 
covered by a rubber dam, which aids in preventing leakage between 
the chamber and skin. A central circular area 5 mm. in diameter 
is left open for inspection through the microscope. In using the 
von Kries plate, Lombard has found the optimum dimension for 
his purposes to be 1 mm. square. If larger plates be used, the 
weight is borne disproportionately at the edges. Lombard has 
shown, as may be seen in the following table, great variation in 
pressure in capillaries of different sizes. The measurement of 
capillary pressure in individuals or in pathological conditions can 
hardly be of value, therefore, while we lack means of discriminating 
between the particular type of capillary under consideration. 
Inspection of the table suggests that the grosser methods of von 
Kries, von Basch, and von Recklinghausen measure the pressure 
in the medium-sized and larger capillaries on the arterial side. 

1 Am. Jour. Physiol., 1912, xxix, 335. 
10 



14G 



l ENOUS BLOOD-PRESSURE 



Capillary pressure. 

von Kries, finger, first pallor 

von Basch, hand, complete pallor .... 
von Recklinghausen, hand, first flush . 
von Recklinghausen, hand, complete flush 

Lombard — Largest capillaries 

" Medium capillaries 

Smallesf capillaries, back of hand . 
Smallest capillaries, finger-nail 
" Most superficial and smallest veins 

Subpapillary venous plexus 



Cm. EM). 

51.3 
34.0 to 41.0 
93 . to 99 . 

75.0 
82.0 to 95.0 
48.0 to 61.0 
20.6 to 30.9 
23 . :; to 37.5 

20.5 to 27.0 
13.5 to 20.5 



.Mm. Hg. 

37.7 
25.0 to 30.0 
68.0 to 72.5 

55.1 
60.0 to 70.0 

35.0 to 45.0 

15.1 to 22.7 
17.1 to 27.6 
15.0 to 20.0 
10.0 to 15.0 



At level of heart. 
Cm. H,0. 

5 . 2 

8.8 



\ enoue pressure 

Sewell 4.6 to 

von Basch .... 
von Recklinghausen: 

filled . . . 

empty 
Hooker-Eyster 



Frank and Rch 
Howell . . . 



Mori i y, and Tabora 
Summary . 



14.0 to 22.0 
20.0 to 26.0 

3.0 to 10.0 
a. v. 8.0 

1.0 to 6.0 

4.0 to 13.0 
av. 7 . 6 

1.1 to 8.7 
a v. 5.2 

1.0 to 13.0 



Normal, 
Mm Hg. 

3 . 4 to 3 . 8 
6.5 



2.2 to 7.3 
a v. 5.9 

0.7 to 4.4 

2.9 to 9.5 
av. 5 . 6 

0.8 to 6.4 
a v. 3.8 

0.7 to 9.5 



H 2 o. 



17.0 
7 to 25.0 
av. 13.9 



up to 25.0 



Pathological 



Mm. Hg. 



12.5 

5.1 to 18.4 

av. 10.2 



up to 18 + 



VARIOUS FACTORS INFLUENCING VENOUS PRESSURE. 

The position of a part with relation to the heart is probably the 
most important factor in determining venous pressure. The weight 
of the blood is such that the pressure of one inch of blood is approxi- 
mately equal to 1.9 mm. Hg. or 2.6 cm. H 2 0. It has been shown, 
however, by von Recklinghausen that the veins of the feet do not 
actually exhibit the pressure demanded by calculation upon this 
basis. This is shown in the following table: 

Venous Pressure at Various Levels. 
(Data from von Recklinghausen.) 

Distance 

below In cm. H2O In nun. llg. 

heart in calculated. Measured. calculated. Measured, 

inches. 

Bearl 10 .. 7.3 

Symphysis pubis, sub- 
ject .silting or stand- 
ins; .... w 12 12 .. 31.0 
Foot, subject sitting . 34 102 55 to 80 75.0 40.0 to 59.0 
Foot, subject standing 18 140 79 to 100 L03.0 58.0to73.0 
Foot, subject recum- 

benl 10 8 to 10 7.3 5.9 to 7.3 



This discrepancy von Recklinghausen supposes to be due to 
the action of the muscle masses of the extremities which, bv their 



VARIOUS FACTORS INFLUENCING VENOUS PRESSURE 1 17 

intermittent pressure upon the veins, aided bj the action of the 
valves of the veins, serve to propel the blood up into the vena cava, 
where he supposes the venous pressure actually exhibits its cal- 
culated value. This importance of muscular activity in promoting 
the return of venous blood from the extremities may explain in 
part the discomfort incident to prolonged standing in one position. 
The importance of position in the determination of venous pressure 
is further shown by the fad that raising one arm above the level 
of the head increases the venous pressure in the opposite arm. 

Barach and Marks 1 have noted thai readings of venous pressure 
in the arm do not always sho"R a constant relative difference pro- 
portional to the elevation or depression above or belo\\ the level 
of the right auricle. Hence venous pressure should be measured 
at the level of the right auricle rather than at another level followed 
by correction to the level of the auricle. 

Changes in arterial pressure do not readily alter the venous press- 
ure. The capillary pressure, at least of the smaller capillaries, is 
much more dependent upon venous than upon arterial pressure. 
Hooker finds that there is no relation between venous pressure and 
changes in pulse rate, and that local changes in vascular tone (cold, 
heat, etc.), do not alter the venous pressure in the hand. Burton- 
Opitz 2 was able to show only a very slight fall of venous pressure 
in the external jugular of a dog upon occluding a portion of the 
arterial supply to the head. 

Normal Venous Pressure at the level of the right auricle was found 
by Barach and Marks to range in the erect posture between 8 and 
18 cm. H 2 and in the recumbent posture between 3.5 and 11 cm. 
H 2 0. Muscular exertion either general or local was found by 
Hooker and 'Wolfsohn, 3 Elfers 4 and Schott, 5 to increase the venous 
pressure from a slight rise up to 14 cm. H 2 0. Hooker 6 has noted 
a distinct diurnal variation under normal conditions of health even 
in individuals confined to bed. He observes a gradual rise through- 
out the day from 10 to 20 cm. H 2 to an average diurnal pressure 
of 15 cm. and a fall during sleep to as low as 7 to 8 cm. During 
sleep he has noted a venous pulse of peripheral origin in the veins 
of the hands. Clark 7 found in 4 bed patients without cardiac 
complications, a durnal variation of from 8 to 10 cm. H 2 0, the 
maximum (10-16 cm.) being reached from 2 to 8 p.m., and the 

1 Arch. Int. Med., 1913, xi, 485. 2 Am. Jour. Physiol., 1903, ix, 198. 

3 Ibid., 1909-10, xxv, 24; 1911, xxviii, 235. 

"Inaug. Diss., Kiel, 1911. 

6 Deutsch. Arch/f. klin. Med., 1912, cviii, 537, 

6 Am. Jour. Physiol., 1914, xxxv, 73. 7 Arch. Int. Med., 1915, xvi, 587. 



lis VENOUS BLOOD-PRESSURE 

minimum (5-8 cm.) between 10 P.M. and 6 a.m. This author from 
repeated observation on 14 eases, 6 with decompensation, 8 with 
good compensation, concludes that a venous pressure above twenty 
is pathological. In cardiac cases, the diurnal variation was found 
by ("lark to be reversed, the highest pressure occurring during the 
sleeping hours. Venous pressure continuously above 20 cm. which 
was not lowered by digitalis, was an indication of grave cardiac 
involvement. On the other hand, with a venous pressure below 
I'd .in. no definite change in the pressure was observed from digitalis 
therapy. The venous pressure and the urinary output generally 
showed a significant inverse variation in cases of cardiac decom- 
pensation. Aspiration of pleural fluid and venesection both lowered 
venous pressure as a rule in his series, but after the latter procedure 
the subsequent rise of venous pressure was rapid. 

Effect of Age on Venous Pressure.— Hooker 1 has found the venous 
pressure to be lower in boys than in men of mature years. The 
following table gives the results of his observations on a series of 
cases including fifty observations in each decade of life. The 
pressures are expressed in centimeters of water, referred to the level 
of the heart, and the range of the individual observations and the 
averages are tabulated: 

Venous pressure. 
Years Minimum. Maximum. Average. 

5 to 15 4 15 8.30 

15 to 25 5 22 22.66 

25 to 35 10 31 15.0 

35 to 45 10 29 17.98 

45 to 55 10 29 19.04 

55 to 65 11 35 24.17 

65 to 75 16 39 25.59 

75 to 85 . . ... 14 35 26.0 

These subjects were up and about and not confined to bed. 
Hooker used his method described on page 141 and took as the end- 
point the complete collapse of the vein, whereas Clark (v. s.) used 
as the end-point the pressure at which the shadow of the vein comes 
and goes with slight oscillations of pressure. The latter is probably 
a more accurate method and gives somewhat lower values, but is a 
more difficult end-]>oint to determine. 

Effects of Exercise. Hooker has also studied the effect of exercise 
upon venous pressure, making ;i reading before and a few minutes 
after a competitive run, or during exercise upon a stationary 
bicycle. The results in a series of individuals are shown in the 
following tabulation: 

> \m. Jour. Physiol., L916, xl, 43. 



1 {RIOUS FACTORS INFLUENCING VENOUS PRESSURE 149 

v. no . 
oxei 

26 . . 8 20 

L9 12 -M 

20 15 24 

20 ... 10 24 

39 .... ... .11 28 

29 

Schneider and Sisco 1 studied the venous pressure of six subjects 
by the method of Hooker and Eysteral altitudes of 6000 and 1 1,109 
feet. At the lower altitude they found in 17 men an average venous 
pressure of aboul 16 cm. of water. En 5 ou1 of 6 subjects the venous 
pressure was lower at the higher altitude bj from 25 to 87 per cent., 
in 2 of the subjects being a1 times slightly negative. In a later 
study- they have shown that physical work causes a greater rise 
in the venous pressure at the higher altitude than at the lower 
altitude or at sea level, but in spite of this fact the maximum pressure 

reached is usually less than at the low altitude because of the lower 
initial venous pressure when at resl at the high altitude. 

Respiration. — Burton-Opitz made careful studio of the effect 
of respiration upon the venous pressure in the external jugular of 
a dog, and found that with expiration the jugular pressure rose 
and that during the pause following expiration it began to fall and 
continued to fall throughout the early part of inspiration, a curve 
similar, therefore, to that of the arterial pressure in the respiratory 
phases. Upon expiration the intrathoracic pressure rises and the 
venous blood does not readily enter the thorax, hut being dammed 
hack causes rise of peripheral venous pressure. Upon inspiration 
the intrathoracic pressure falls and the venous blood flows readily 
into the thorax, with fall in the peripheral venous pressure; near 
the thorax the venous pressure may he negative during inspiration. 
The respiratory variation found in the external jugular pressure 
is as much as 3.8 em. H 2 0, and heeomes greater as the thorax is 
approached. The opening of the thorax by increasing the intra- 
thoracic pressure (which is normally less than the atmospheric) 
causes a prompt rise of venous pressure of from 1.5 to 3.5 cm. H 2 0. 

Cardiac Action. — Impaired cardiac action by leading to venous 
stasis produces an increase of venous pressure. Experimentally, 
stimulation of the peripheral end of the sectioned vagus produces 
a slight rise of venous pressure. Clinically, any form of myocardial 
decompensation leads to increase of venous pressure which may 

1 Am. Jour. Physiol., 1914, xxxiv, 1. 

2 Ibid., 1916, xl, 3S0. 



150 VENOUS BLOOD-PRESSURE 

rise to 30 cm. II 2 in the veins of the arm at the cardiac level. 
Indeed, increased venous pressure may, in the early stages, be the 
only sign of circulatory stasis. 

Intravenous Injection. — That intravenous injections increase the 
venous pressure more proportionately than they do the arterial 
was shown by Bayliss and Starling. 1 Rise of venous pressure at the 
heart also results from abdominal pressure, bandaging or elevation 
of the extremities, or from elevation of the abdomen above the 
level of the heart. The importance of venous pressure in relation 
to cardiac output has already been discussed. Experimentally 
as a result of therapeusis, a rise of venous pressure occurs after large 
doses of epinephrin, pituitrin, and alcohol, not after digitalis, 
strophanthin, strychnin or caffein. This rise is proportionate to, 
and apparently the result of disturbed heart action. It is therefore 
apparently simply a stasis reaction and not the result of vasomotor 
influence. A fall of venous pressure may follow the administration 
of the nitrites or large doses of morphin, and since cardiac func- 
tionation remains unimpaired, may be attributed to a direct 
influence on the vasomotor mechanism. 2 

1 Jour. Physiol., 1894, xvi, 159. 

2 Capps, J. A., arid Mathews, S. A.: Venous Blood-pressure as Influenced by the 
Drugs Used in Cardiovascular Therapy, Jour. Am. Med. Assn., 1913, lxi, 388. 



( II \ PTEB V. 

THE FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

AS DETERMINABLE BY BLOOD PRESSURE 

ESTIMATION AND ALLIED TESTS. 

In the following chapter are described a number of methods 
which have been suggested in the hope of throwing inure Light on 
the question of the functional efficiency of the circulation. Most 
of them are based on sound theoretic principles, and would be 
invaluable if our instrumental measurements were sufficiently 
exact ami comprehensive to insure an accurate basis for our deduc- 
tions. Unfortunately, however, the data obtainable by sphygmo- 
manometry, etc., are, even when collated with the greatest care, 
subject to unavoidable sources of error, and hence our resultsare 
only approximate. To use such data as a basis for elaborate 
calculations, entailing the use of involved mathematic and algel raic 
formulae for the elucidation of the complex factors included in the 
static and dynamic laws of the circulation, only magnifies our errors 
and often leads to a veritable reductio ad absurdum. Thus far it 
must be admitted no entirely satisfactory method has been perfected, 
mainly because we cannot measure vascular tonus, or estimate 
the role of psychic processes. Furthermore, to yield definite 
indications many of the tests have to be carried to a point at 
which concomitant symptoms and ordinary physical signs are of 
themselves sufficiently evident criteria of functional insufficiency. 
Unquestionably, however, some of the methods about to be de- 
scribed do throw a useful light on the problem under consideration, 
especially if the results thus obtained are accepted with due reserve. 

Many are the attempts which have been made and numerous 
the methods suggested for determining the functional capacity 
of the heart. The importance of this subject from a diagnostic, 
prognostic, and therapeutic stand -point cannot be overestimated. 
Such procedures as are based in part, at least, upon blood-pressure 
measurements will be here considered. 

Generally speaking, such tests depend upon the way in which 
the pulse rate and blood-pressure both respond — quantitatively, 



152 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

qualitatively, and temporarily— to definite amounts of muscular 
exertion or to change of posture (see p. 51). This subject has been 
extensively studied by Masing, Buttermann, Christ, Staehelin, and 
others. 1 The work performed was either definitely measured with 
various tonus of apparatus, or roughly estimated by such tasks as 
lifting, stair-climbing, walking, etc. 

"In blood-pressure and exercise we have an unfailing guide to 
the true condition. Whatever the abnormality, the great question 
is the integrity of the heart muscle, the reserve force of the heart, 
for upon this chiefly depends the prognosis. The pulse should be 
counted, the heart examined, and the blood-pressure taken, and 
then with the cuff attached to the arm, the applicant should be 
exercised to the equivalent of climbing two flights of stairs and 
then reexamined quickly. Exercise when not too severe will regu- 
late the pulse if the condition is simple. If serious disease is present 
the irregularity will be greatly increased. If the heart muscle is 
in prime condition the systolic pressure will jump 15 to 40 mm. 
and, tested every two minutes, will be found to resume its 
original place in six to eight minutes. If the condition is bad, in 
a powerful effort of the heart to respond, the rise may be even 
greater, but the return will be exceedingly slow, sometimes requir- 
ing twenty to thirty minutes. If the state of the muscle is ex- 
tremely bad and the reserve force exhausted, the systolic pressure 
may fall instead of rising and the diastolic remain stationary, or 
rise a little, creating a very small pulse-pressure. It will be a long 
lime before graphic instrument tracings are required in life insur- 
ance, if ever, but we have in exercise and blood-pressure a thor- 
oughly reliable test, and it is the duty of the examiner to be safe 
in his recommendation of every applicant." 2 

Crampton's Test of Vasomotor Efficiency- In rising from the 
recumbent to the erect posture blood-pressure tends to fall as a 
result of gravity. Unless this tendency were automatically regu- 
lated, syncope would occur as a result of cerebral anemia. In a 
normal vigorous man, however, such a change of position causes a 
rise of blood-pressure amounting to 8 to 10 mm. Hg. This increase 
may result from increased vasomotor tone or from increased cardiac 
work, or as a result of both factors. Bearing these facts in mind 
Crampton 8 has devised the following table to test vasomotor effi- 

1 For bibliography, sec Norris, CI. W.: The Functional Capacity <>f the Heart. 
Internat. Clinics, 1907, 17th series, vol. i. 

Lankford, .1. 8.: The Hearl id Life insurance, Med, Rec, ( Ictober 17, 191 1, p. <'.s7. 
Blood Ptosis, New York Med. .lour., November 8, L913. 



CRAMPTON'S TEST OF VASOMOTOR EFFICIENCY L53 

ciency through the observation of pulse rate and blood-pr< 
responses to postural change. The tables while setting whal is 
perhaps a high normal have shown thai vasomotor tone in the same 
individual varies greatly as a resull of mental or physical fatigue, 
infectious processes, etc. It may be used with especial edification 
in the study of essential hypotension cases. 

The Technic- "The sphygmomanometer is adjusted over the 
brachial artery and the patient is placed on a comfortable couch 
with a low pillow. The heart rate i counted by quarter-minutes 
and a gradually decreasing rate is usually observed. Counting 
should continue until two successive quarter-minutes are the same, 
this is multiplied l>,\ 1 and recorded. The systolic pressure i- then 
taken preferably l>y auscultation. The patienl stands, the heart 
rate is counted as before until it reaches the 'standing normal,' 
when it is recorded, and the blood-pressure i> then taken. The 
differences arc calculated and reference i> made to the scale. 

"For example Case XX: L. V., age seventeen years, said to 
be in good condition at 11:20 a.m. 

Pulse rate. Blood-pressure. 

Horizontal - . . . . 68 100 

Vertical 104 94 

Difference +3G -G 

Percentage record, 20. 



"This is a very poor record taken from an apparently normal, 
strong young football player of exceptional ability who had previ- 
ously given records above SO. 

" I was at a loss to account for this, for questioning failed to bring 
out any history of loss of sleep, dissipation, or illness. He looked 
quite as 'fit' as usual. He was absent next day, and remained 
home for a week with a 'cold and fever.' It is evident that the test 
revealed a weakened vasotone, the beginning of actual illness before 
any other symptom could be noted. Others who have used this 
test have noted similar cases." 

If the vasomotor tone is deficient, the heart must make up for 
it by an increase in rate — the greater the increase, the less efficient 
the vasomotor tone. 

"The usual range of the systolic pressure is from +10 to —10 
of the heart-rate increase from to 44, as observed from records of 
a large number of cases. Upon a statistical balancing of these two 
series of frequencies, and assigning equal percentages to equal 
ranges, the following scale is constructed : 



154 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

PERCENTAGE SCALE. 
Vasomotob Tone. 











Blood-preesure. 


















Increase 








Decrease 




Heart-rate 






















+ 10 


+s 


+6 


+4 


+2 


-2 


-4 


-G 


-8 


-10 


to 1 . 


. 100 


95 


'.ill 


85 


80 75 


70 


65 


60 


55 


50 


5 to 8 . 


. 95 


90 


85 


80 


75 70 


65 


60 


55 


50 


45 


9 to 12 . 


. 90 


85 


80 


7.-, 


70 65 


60 


55 


50 


45 


40 


13 to 16 . 


. 85 


80 


75 


70 


65 60 


55 


50 


45 


40 


35 


17 to 20 . 


. 80 


75 


70 


65 


60 55 


50 


45 


40 


35 


30 


21 to 24 . 


. 75 


70 


65 


60 


55 50 


45 


40 


35 


30 


25 


25 to 28 . 


. 70 


65 


60 


55 


50 45 


40 


35 


30 


25 


20 


29to32 . 


. 65 


60 


55 


50 


45 40 


35 


30 


25 


20 


15 


33 to 36 . 


. 60 


55 


50 


45 


40 35 


30 


25 


20 


15 


10 


37to40 . 


. 55 


50 


45 


40 


35 30 


25 


20 


15 


10 


5 


41 to 44 . 


. 50 


45 


40 


35 


30 25 


20 


15 


10 


5 






Note. — In rase of increase in pressure higher than 4-10 add 5 per cent, to the 
+ 10 column for each 2 millimeters in excess of 10. 

"This scale provides a convenient and intelligible method of 
recording and reporting cases and permits a numerical statement 
of the function in question. Its 100 mark indicates a perfectly 
efficient working of the vasomotor system under test, the zero is 
approximately the point where the average person is unable to 
maintain the erect posture." 

Among 116 athletes R. Tait McKenzie found the postural change 
in pulse rate and systolic blood-pressure average as follows: 

Number ol 
studi i Lying. 

34 78 

28 75 

30 83 

24 70 

116 77 84 116 115 

It will be noted that there was a very constant variation in the 
pulse rate amounting to about seven beats per minute between the 
two postures. The blood-pressure findings were much more variable 
and when an average was established they were practically identical 
in the two positions. Among 3S8 students with cardiac abnormal- 
ities arrhythmia, murmurs, etc. — the systolic blood-pressure aver- 
age was somewhat higher (138+ mm. Ilg.) than among the athletes 
with normal hearts. 

Passive change of posture. 

"When the element of muscular effort has been eliminated, 
change of bodily posture from the erect to the horizontal will cause 
an increase in the maximum pressure, a decrease in the minimum 



Ise. 
Standing. 


Bloo 
Lying. 


d-pressure. 

Standing. 


86 


114 


113 


85 


120 


121 


85 


120 


114 


79 


110 


114 



CRAMPTON'S TEST OF VASOMOTOR EFFICIENCY L55 

pressure, and an increase iii the pulse-pressure. After five minutes 
in the horizontal posture when the subject is retilted to the erecl 
posture, the maximum pressure \\ ill diminish, the minimum pre sure 
increase and the pulse-pressure diminish. It will be rioted thai in 

both instances the pulse-pressure follows tin- same trend :i^- the 

maximum pressure. Change of posture from the erecl to the hori- 
zontal causes a fall in the venous pressure. < lhange of posture from 
the horizontal to erect causes an increase of the venous pressure." 1 
Among twenty healthy young adults change of posture yielded 
the following results: 











Head 


Righl 


Left 


Systolic pressure. 


Standing. 


Sitting. 


Supine. 


down. 


lateral. 


lateral. 


Right arm 


. 132. G 




l.vj :, 


L66 2 


1 55 . ( i 


1111.11 


Average . 


. L30.8 


L31.7 


L50 i 


L65.6 


l 13 5 


L33.0 


Left arm . 


. L30.0 


130.0 


l 18. 3 


L65.0 


141.0 


L56 


Pulse rate 


86 


82.0 


68.7 


65.8 


68 l 


69. 1 



In other words, "Blood-pressure increases in the brachial arteries 
from the standing to the head-down position, inclusively in the 
following order: standing, sitting, left lateral, right lateral, supine, 
head down." 2 

During muscular exercise we see an increased respiratory gas 
interchange, the amount of which may exceed that occurring dur- 
ing rest over twentyfold. Associated with this there is a marked 
increase in the rate of .blood flow, so that the normal circulation, 
the time of which is fifty-five seconds, may be reduced to five 
seconds during exercise. Such changes must, of course, produce 
enormous alterations in blood-pressure values. 

Muscular exertion may be accompanied either by a fall or by a 
rise of pressure, and it has been found that the more fit and well- 
trained the animal the less the tendency for the pressure to rise. 
Thus in horses and in well-trained athletes there is a fall. The 
average man shows a primary rise, followed by a fall upon cessa- 
tion of work. The more strenuous the work and the less trained 
the man, the greater and the earlier will be the fall. This may 
result from cardiac weakness or may be a result of Nature's safe- 
guard against cardiac overstrain, the fall of pressure being brought 
about reflexly through the agency of the depressor nerve. During 
youth both pulse and blood-pressure are more labile during exer- 
cise and tend to keep pace with each other. In adults there is less 

1 Barach, Joseph H., and Marks, W. L. : Effect of Change of Posture without 
Muscular Exertion on the Arterial and Venous Pressures, Arch. Int. Med., May 
15, 1913, ii, No. 5. 

2 Stephens, O. Z.: Blood-pressure and Pulse Rate, Jour. Am. Med. Assn., 1904, 
xliii, 955. 



L56 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

tendency for the pulse and more for the pressure to rise. In health 
both pulse and pressure return promptly to the normal upon the 
cessation of work. With a diseased cardiovascular system this is 
aol so promptly accomplished. The heart which has been weak- 
ened by infectious processes shows a wide range and a prolonged 
duration of pulse and blood-pressure variations. The amount of 
psychic effort required is of the greatest importance. Work which 
is performed passively, automatically, without any particular 
psychic concentration, is not accompanied by a rise in tension. 
The primary fall of pressure which occurs under training is largely 
the result of eliminating the volitional psychic factor. An increase 
of pressure under muscular work depends more on the cerebral 
stimuli required than on the amount of work done. In the hyp- 
notized subject, imaginary work produced an elevation of pressure 
to 200 nun. Hg. (Klemperer). These causes explain many of the 
failures of toting functional capacity by measured amounts of 
work. Although we can measure the work performed in kilogram- 
meters we have no means of estimating the amount of nervous 
force and psychic energy which may be expended upon the same 
task by different classes of trained and untrained, nervous and 
phlegmatic, energetic and lazy individuals (see p. 384). 

The increase of pressure which is associated with muscular effort 
affects chiefly the systolic pressure; the diastolic element tends to 
lag behind, thus increasing the amplitude of the pulse. On assum- 
ing the ered posture the minute volume decreases slightly, the 
systolic output greatly (20 per cent.). In the recumbent posture 
the minute volume in women increases 17.2 per cent., and the 
systolic output ill per cent. In men this change was not observed 
owing probably to a more efficient vasomotor system. 1 Lowsley 2 
found that physical activity caused a rapid rise in blood-pressure 
which precede, the increase of the pulse rate. During continued 
exercise these curves show but little change. After cessation from 
work the fall in the systolic pressure again precedes the decrease in 
the pulse rate. A secondary rise of the pulse rate occurs which is a 
"reflex effect due to low blood-pressure of the subnormal stage." 

Muscular effort sufficient to increase the pulse rale provokes a rise 
of the systolic, diastolic and the venous pressures. Inasmuch as the 
systolic pressure rises more than the diastolic, the pulse-pressure 
is increased. 

1 Lindhard, .1.: Effect "i Posture on the Outpul of tin- Heart, Skand. Arch. f. 
.. L913, xxx. 395. 
The Effects of Various Forms of Exercise on Systolic, Diastolic, and Pulse Pres- 
sures and the Pul R be Lm. Jour. Physiol., 1911, xxvii, 446. 



GR \i r\ ER'S TEST L57 

Following the primary maximal rise of systolic pressure a gradual 
decline occurs, but while exercise is being continued the pressure 
never reaches the normal level. The diastolic pressure generally 
follows the systolic curve bu1 its maximum is reached later and 
upon cessation from work it invariably falls belo^ it- normal level. 
According to Lowsley the longer the subnormal diastolic phase, 
the greater the circulatory fatigue. The venous pressure shows 
often a sudden drop to normal after cessation from exercise. Exer- 
cise associated with strain requiring a closed glottis and a rigid chesl . 
disproportionately increases blood-pressure in relation to the pulse 
rate and very markedly increases venous pressure. 

The Auscultatory Phase Test. Goodman and Howell su£ 
that by recording the relative length of the five auscultatory phases 
certain deductions regarding myocardial efficiency could he drawn. 
They group the second and third phases as factors of cardiac 
strength (C. S.) and the first and fifth phases as factors of cardiac 
weakness (C. W.), >'■ </•> i" =' given case with a pulse-pressure of 
45, the first phase constituted 31.1, the second 14.4, the third 11.1, 
the fourth 13.3 per cent, of the total. Therefore, 

('. S. : C. W. :: 55.5 : I 1. 1. 

Swan, 1 who has employed this method in 72 cases believes it is 
capable of yielding useful information regarding myocardial strength 
at the time the observation is made. 

A second phase which forms more than 10 per cent, of the pulse- 
pressure, and a C. S. : C. W. ratio in which the former i- greater 
than the latter, bespeaks a competent myocardium. When com- 
pensation is deficient the C. S. — C. W. ratio often cannot he studied, 
owing to an absence of one or more phases. When this is the case 
the length of the second phase may he taken as a criterion of effi- 
ciency. "A long second phase indicates a good heart muscle." 

Graupner's Test. — Graupner 2 endeavored to test cardiac func- 
tionation by noting the effects of measured work upon the pulse, 
the blood-pressure and the size of the heart, the blood-pressure 
being measured with a Gartner tonometer and taken when the 
pulse had reached the same rate, after the exercise, which it had 
before this was commenced. His investigations led him to the fol- 
lowing conclusions: (1) Blood-pressure remains constant — cardiac 
sufficiency. (2) Blood-pressure falls — cardiac insufficiency. (3) 

1 The Auscultatory Method of Blood-pressure Determination, A Clinical Study, 
Internat. Clinics, IV, Series 24. 

2 Graupner: Die Mechanische Priifung und Beurtheilung der Herzleistung, 
Berliner Klin., 1902, xv, No. 174; Deutsch. med. Wchnschr., 1906, xxxii, 1029. 



158 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

Blood-pressure rises, but returns to normal — compensatory capac- 
ity. 1 Blood-pressure rises, falls rapidly, -without a tendency to 
rise again fatigue. 

Barringer's Test. — More recently Barringer 1 has studied the effect 
of measured exercise upon the pulse rate and the blood-pressure. 
The exercise consisted either in lifting dumb-bells or in riding a 
bicycle ergometer of the Krogh and Linhard 2 type. He found that 
the functional capacity of the heart may be judged by the form of 
the systolic blood-pressure curve after the completion of the 
work. 

Ordinarily as a result of active exercise the pulse rate increases 
and blood-pressure rises in proportion to the work performed. 
Upon cessation of work both pulse and pressure return to the normal. 
" If the systolic blood-pressure reaches its greatest height not imme- 
diately after work but from thirty to one hundred and twenty 
seconds later, or if the pressure immediately after work is lower than 
the original level, that work, whatever its amount, has overtaxed 
the heart's functional capacity, and may be taken as an accurate 
measure of the heart's efficiency." This delayed rise of systolic 
pressure does not as a rule vary with the muscle groups employed 
farms or legs). Barringer explains the foregoing phenomena by the 
following physiological facts: Muscular work increases the carbon 
dioxide in the blood; this stimulates the nerve centres controlling 
the suprarenal glands and hence an increased adrenalinemia results 
which constricts the splanchnic vessels and raises blood-pressure. 
The latter is abetted by the increased cardiac rate. After exercise 
the carbon dioxide diminishes and normal values are reestablished. 3 
In other words, with an individual at rest, the heart only discharges 
one-half of its ventricular content with each systole, but under 
the stimulus of exercise and when more blood is brought to it from 
the muscles the entire ventricular content is promptly expelled 
and hence the heart becomes smaller. In normal individuals hard 
work rapidly increases the systolic pressure as a result of which the 
ventricle, when fatigue occurs, fails to completely discharge its 
content. Upon cessation from work the splanchnic vessels relax 
and blood-pressure falls, hence the ventricle again begins to empty 
itself completely. This increased output overshadows the splanch- 

1 Barringer, T. B., Jr.: The Circulatory Reaction to Graduated Work as a Test 
of the Heart's Functional Capacity, Arch. Int. Med., March, 1916, xvii, 363. 

*Skand. Arch. f. Physiol., 1913, xxx. :>,7s. 

'Cannon: Am. Jour. Physiol., 1914, xxxiii, 356. Von Anrep: Join*. Physiol., 1913, 
si v, 318. Hooker: Am. Jour. Phyaiol., 1911, xxviii, 235. Schneider and Havens: 
Ibid., 1915, xxxvi, 239. 



BARRINGER'S TEST 159 

nic dilatation and hence pressure temporarily rises, thus explaining 
the delayed rise in blood-pressure. 

In patients with cardiac disease the systolic rise during exercise 
is slight and the fall of pressure often begins during the period of 
work. The curve after work is similar to that occurring in normal 
subjects but much less muscular work is sufficienl to develop the 
delayed rise. 

Method of Performing Barringer's Test of I he Heart's Functional 
Capacity. — "The apparatus used consists of pairs of 5-, L0-, 15- and 
20-pound dumb-bells, and a steel bar aboul 10 inches long weighing 
25 pounds. Two types of movements are done with the bells. In 
the first a pair of dumb-bells is held at the shoulders, one in each 
hand, and then pushed alternately above the head and toward the 
median line until the arms are fully extended. As one bell moves 
up fairly rapidly the other bell returns to the shoulder, the tun 
moving in a sort of see-saw rhythm. In the other movement a bell 
is held in each hand, the arms hanging by the side of and close to 
the body, and then each forearm is alternately flexed, raising the bell 
to the shoulder. The patient stands or sits according to his con- 
dition. But one movement is performed with the steel bar. It is 
picked up from the floor with both hands, raised first to a level with 
the shoulders, then pushed above the head until the arms are fully 
extended and then quickly lowered to the floor again with a single 
rapid motion. 

"It is possible to calculate approximately the number of foot- 
pounds of work performed in each of these movements. There is 
a certain amount of work, however, which we cannot estimate in 
foot-pounds. When a patient stands with a pair of dumb-bells at 
his shoulders without moving them, work is done as shown by his 
circulatory reactions, but we cannot estimate it in foot-pounds. 
This unknown factor can be ignored, however, for our purpose. 

"Most adults average 2 feet as the distance through which a 
bell is pushed from the shoulder to full extension of the arm. In 
the flexion movement, the distance through which the bell is car- 
ried from the side of the body to the shoulder averages from 2 feet 
to 2 feet 6 inches. Now if a 5-pound bell is pushed through 2 feet, 
10 foot-pounds of work are done. If the total number of pushes 
are twenty, 200 foot-pounds are done. For the sake of comparison, 
the time it takes a patient to do any quantity of work should be 
noted. 

" If the patient whose heart is to be tested has but recently recov- 
ered from an attack of cardiac insufficiency, it is well to start with 



1G0 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

a pair of 5-pound bells, the patient sitting on a stool. Two hun 
dred foot-pounds of work are then given cither by flexing or extend- 
ing the bells. The pulse rate and blood-pressure are taken every 

thirty seconds. 

"After the pressure and pulse have returned to the original, 300 
or 100 foot-pounds are done in the same way. The work is increased 
with each experiment until we reach a delayed rise in blood-pressure. 
The experiment which has caused a delayed rise should always be 
repeated after a few minutes' rest, with, a slightly increased amount 
of work, for the purpose of confirmation. When once the amount of 
work which will produce a distinct delayed rise in blood-pressure 
is ascertained, it is quite remarkable how little the results vary 
on a repetition of the experiment with the same or increased work. 
Yet if our test is valid this should be so. 

"The following examples illustrate this point: 

"This patient was sixty-four years old and suffered from aortic 
regurgitation and cardiac insufficiency. 



Pulse rate 



Systolic blood-pressure 



1G0 foot-pounds (10-pound bell extended eight times) 



3.45 . 


80 


3.46 . 
3.46! 

3.47 . 


88 

80 


80 


3.47| 
3.48 . 


80 


80 


3.49 . 


80 


3.49 . 


80 


3.55 . 


80 


3 56 


200 foot-pounds (10-pound bell exte 
88 


3.56| 
3.57 . 


. 84 


80 


3.57! 
3.58 . 


76 


. . . 76 

so 


4 03 


80 


4.04 . 


240 foot-pounds (10-pound bell extern 

88 


1 ii I ! 


s| 


4.05 


. . . . 84 


1 05 j 


80 


4.06 . 


80 


4.06! 
4.07 . 


76 


80 


4.08 


76 


4.09 


76 


t.13 


76 



Delayed rise 



Delayed rise 



132 
138 

134 
134 
132 
134 
134 
134 
130 



L36 

1 12 
138 

l l l 
l I l 
138 
l 11 
134 
l-.'s 
130 



"As a general rule a patient's cardiac capacity will vary but slightly 
from day to day. If he improves in general condition his cardiac, 



KATZENSTEIN'S TEST 



mi 



capacity increases, and it' lie retrogrades h decreases. Lack of sleep 

or transienl infections have very pr p1 and decided effects on the 

fan line capacity , particularly in persons who already have damaged 
hearts. 

"Patients showing a delayed rise of pressure with work amount- 
ing to less than LOO foot-pounds per minute, usually present other 
signs of cardiac insufficiency. An exception to this statemenl occurs 
in aged subjects. Capacities ranging between H»n and 1000 foot- 
pounds are mel with in patients who can walk shorl distances. 
Tests of less than 1000 foot-pounds per minute may be construed 
as confirmatory of a myocardial lesion." 1 



120 


d 








110 / 




100 / 


\_ 




00 






60 jiy 






r 





a 








6 



Fig. 69. — The absolute sphygmogram. If the cuff pressure be raised to 100 mm. 
Hg. only that part of the pulse wave which is in excess of this pressure will be traced 
(see page 163). 

Katzenstein's Test. — This test for determining the degree of func- 
tional capacity of the heart is based upon the manner in which this 
organ responds to compression of both iliac arteries. 2 

Experimentally in animals, if some of the large vessels are oblit- 
erated, blood-pressure rises while the pulse rate remains stationary. 



1 Barringer, T. B. : Studies of the Heart's Functional Capacity as Estimated by 
the Circulatory Reaction to Graduated Work, Arch. Int. Med., 1916, xvii, 670. 
2 Katzenstein: Berliner klin. Wchnschr., 1907, xliv, No. 16. 
11 



102 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

In human beings it was found that if the heart was functionally 
potent, bilateral obliteration of the iliac arteries, maintained for 
from two to five minutes, caused a rise in blood-pressure of from 
."> to 15 mm. of mercury; the pulse rate remained stationary or 
even diminished. In the case of an hypertrophied heart, with 
good compensation, the blood-pressure rises perhaps to 40 mm., 
the rate being still unaffected. If there is slight insufficiency, the 
pressure does not rise, whereas the pulse dors become accelerated. 
In severe insufficiency the pressure falls and the pulse becomes 
nil ire rapid. These tests are made with the subject in the recumbent 
posture. The sources of error in this method are manifestly mental 
excitement, and the possibility of producing pain during the com- 
pression of the arteries, either of which might seriously militate 
against the accuracy of the results; but with due care both of these 
factors may be eliminated. 

With a view toward investigating Katzenstein's test, the author 1 
studied a number of cases both among healthy individuals and 
among those in whom cardiac weakness or disease was assured. 
As the result of these investigations it was found that, generally 
speaking, the cases responded to the test as has been contended 
by the deviser of it. There were, however, notable exceptions in a 
number of instances. Although the majority of cases with manifest 
cardiac weakness responded positively to the test, yet — and here 
lies the main ground for objection— many of them did so in such 
equivocal terms, that is, by such small changes in the pulse rate or 
blood-pressure, that the final decision was left largely to the per- 
sonal equation of the observer. Morelli 2 suggests that compres- 
sion be exercised by means of inflated rubber stockings. In a 
recent communication based upon three thousand cases, during 
the lasl ten years, Katzenstein 3 reiterates his belief in the efficacy 
of his test. lie has found it of especial value in discovering cardiac 
weakness in operative cases in which chloroform was subsequently 
used as an anesthetic. 

This test has been investigated by numerous writers. It may at 
times have some corroborative value, but much dependence should 
not be placed upon it. A test based on the same general principle 
has been suggested by Mosler, 1 who estimates the blood-pressure 

1 N'urris, G. W.: The Functional Capacity of the Heart, Internat. clinics, vol. i, 
Series 17. 

Delia Capacita Funzionale del cuore e <l«'i Vasi Sanguini, Bull. Soc. Med. C'hir. 
di Pavia, March 12, 1910. 

Duetsch. med. Wchnschr., 1915, vol. xli, No. 16. 
4 Dor Atemstillstand in defer [nspirationsstellung: Ein Versuch z. Beruteilung 
der Kreialauffunktion, Ztschr. f. Win. Med., 1913, Lzxviii, L33. 



THE VENOUS PRESSURE TEST 



163 



after ;i deep forced inspiration at the conclusion of which the breath 
is held. 

The Venous Pressure Test (Schott's 1 Test). It appears that in 
health if the patient raises his arm to an angle of 60 degrees while 
1\ ing quietly without any other muscular effort, the venous pre ure 
shows on an average an increased pressure of 0.5 cm. II () some- 
times no increase, or even a fall). In well-compensated heart 



850 H 


■ II 1 1 1 1 1 1 

X 


240 


K 


^.M 


\ 




\ 


210 


\ J 








.' 


\ 










\ 








i 


\ 






\ 






















\ v 




1 








19 
















1 












rM 1 








ITS! 




















































































Fig. 70. — Absolute sphygmograms and pulse tracings from a case of marked 
hypertension and from a case of marked hypotension. Showing that the pulse 
tracing gives a very inaccurate representation of the actual height of the arterial 
pressure. (After Gallavardin.) 

lesions the increased pressure averages 2.3 cm.; in broken compen- 
sation, 4 to 7 cm.; in conditions of anasarca, etc., 7.3 cm. He there- 
fore considers figures above 3 cm. as pathological. Passive eleva- 
tion of the limb produces no increase of venous pressure. 



1 Die Erhohung des Druckes in venosen System bei Anstrengung als Mass fur 
die Funktionstuchtigkeit des menschlichen Herzens, Deutsch. Arch. f. klin. Med., 
1912, cviii, 537-553. 



164 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

The Absolute Sphygmogram. The information obtainable from 
the pulse tracing alone so far as blood-pressure is concerned, is 
slight because: 1 I we do not know the actual value of the abscissa 
and (2) because the actual length of the waves depends largely on 
the adjustment of the sphygmograph (amount of pressure exerted 
on the underlying artery). 





.. 








1 — 












































































too 


\ 










































I- 












































'■ I \ 






































x 




































\ 


































\ 














































































































.1\ 








ll<> 




















:< 


































































■i 




























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61 








































K) 




























































10 
































" 









































































Absolute sphygmogram and pulse tracing from a case of hypertension 
and from a case of hypotension. (After Gallavardin.) 



In I'.iol Sahli suggested a method for plotting the sphygmogram 

in absolute pressure values. His method depends upon the fact 
that if sphygmograms are taken from the radial artery while a 
blood-pressure .nil' is applied to the brachial artery above with 
increasing pressures, the sphygmogram will be traced of only that 
portion of the pulse curve corresponding to intra-arterial pressures 
higher than the pressure in the cull'. Thus, if Fig. 69 represents, 
tli«' actual pressure curve of the pulse in the artery, if the pressure 
in the cuff be raised to 100 only that portion of the pulse curve 
drawn heavy and corresponding to pressures above 100 will be 
traced. It is therefore possible, by altering the pressures in the 



THE BLOOD PRESSl RE Ql 01 II. \ 1 



L65 



cuff and noting the amount of the sphygmogram traced a1 each 
pressure, to determine the absolute pressure of any poinl on the 
pulse curve. 

The time relations of these points maj be determined from the 
sphygmogram. The curve maj then be plotted on cross-section 
paper, allowing the vertical lines to represenl time units and the 
horizontal lines units of blood-pressure. It is only from such a 
curve thai the true mean pressure can be determined. Thus, it' 
the length of a sufficient number of equally spaced vertical lines 







"H 1 i~tu 1 












f\ 




3 i 




















SI 3Sl 1 \ 


C I 




_ii'_ 




/ \ 








1 \ 












\ 


































n 












.1 




10 


















-■ 
















Fig. 72. — Showing absolute sphygmogram and pulse tracing from a suDjec. . 
normal blood-pressurp, and that of a case of nephritic hypertension. (After Galla- 
vardin.) 



a subject with 



from the base line a-b to the pressure curve c, d, e, f, g, be measured 
and their average taken, such average will be the true mean pressure. 
For clinical purposes Sahli constructs a simplified form by plotting 
only the systolic pressure or crest of the pulse curve (d), and the 
diastolic pressure or lowest point of the pulse curve (c and g), thus 
obtaining the dotted figure a, c, d, g, b. From such a diagram one 
can judge accurately as to the quickness or slowness of the pulse 
(pulsus celer, or pulsus tardus). 

The Blood-pressure Quotient. — Let us assume that the data 
obtained regarding systolic and diastolic pressures are correct. 



166 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

What conclusions are we warranted in drawing regarding the 
amount of work performed by the heart and the amount of its 
systolic output? The question has recently been ably summarized 
by O. Midler, 1 from whose article I have freely drawn. 

Tigerstedt has shown that the pulse-pressure divided by the systolic 
pressure is of value in estimating the part played by vascular 
resistance and cardiac work respectively in changing circulatory 
conditions. 

The rationale of the method is as follows: With increased cardiac 
work, the pulse-pressure as well as the systolic pressure increases. 
If, on the other hand, peripheral tonus alone increases, the systolic 
pressure rises, while the pulse-pressure falls. Vasodilatation pro- 
duces a fall of systolic pressure and an increase of pulse-pressure. 
Therefore if the systolic pressure and the pulse-pressure move in 
the same direction and proportionately, the cause lies in the heart; 
if in the reverse direction, or not proportionately, the cause lies at 
least partly in changes in vascular tonus. The cardiac element is 
also indicated by the number of systoles. 

■a •,, ~ Pulse-p ressure . „ , . 

B. P. Q. = -= — , ,. — — = (normally about 0.3) 

Systolic pressure 

1. A changed systolic pressure while the quotient remains the 
same points to a change in the work of the heart. If both systolic 
and pulse-pressure rise, an increased; and if both fall, a diminished 
cardiac activity may be assumed. 

2. When systolic pressure and blood-pressure quotient move in 
approximately equal but opposite directions, indications point to 
an alteration of vascular tone. Thus an increase in systolic pressure 
with a fall of quotient = increased tonus and vice versa. 

3. When systolic pressure and quotient move unequally in the 
same or in opposite directions, both the heart and the vascular sys- 
tem contribute to the effect. With the limitations imposed by the 
response of the pulse-pressure to factors other than the systolic 
output (already considered on page 53), and if our estimation of the 
systolic and diastolic pressures be accurate, these assumptions are 
warranted. The variations of aortic elasticity for different degrees 
of pressure are clinically a negligible quantity. But a far more 
serious source of error lies in the fact that the smaller arteries and 
arterioles possess a distinct tonus, the amount of which we are as 
yet unable to measure. If the arterial system merely consisted 

1 Die unMiiti^c Blutdruckmeeaung u. ihre Bedcutung f. <1. prakt. Med., Med. 
Klinik, January 12, 1908, p. 47 et seq. 



THE BLOOD PRESSURE QUOTIENT L67 

of rubber tubing our figures would certainly be at leasl approxi- 
mately correct, and our deductions correspondingly accurate; in 
illustration of this it has been demonstrated thai in cases of arterio- 
sclerosis the pulse-pressure is often twice as large as in a normal 
individual, but we have no right to conclude from this that in 
such a case the systolic output is correspondingly great. It is far 
more likely in such an instance that, the difference is due to the 
rigidity of the arterial wall. The pulsatory reaction of a contracted 
artery is entirely different from that of a relaxed artery of the ame 
caliber. Again, as F. Eflemperer has shown, if we dip one arm into 
hot and the other into cold water, the pulse-pressure will be found 
to decrease in the former and to increase in the latter; and yet we 
know that cold produces vascular contraction. Which of the two 
sides shall we choose as the index of systolic cardiac outpul ? 

It may be argued in reply that such extremes as the hot- and 
cold-water experiment do not occur under norma) conditions, but 
notwithstanding we must hear in mind the fact that plethysmo- 
graphic studies have indubitably demonstrated the fad thai fre- 
quent and often extensive vasomotor changes are going on more 
or less constantly in the normal human economy, especially as the 
result of pain, psychic influence or temperature change, all of which 
are apt to enter into an ordinary blood-pressure estimation. 

Fuerst and Soetbeer 1 suggest that the Strassburger formula be 
modified to read: 

Pulse-pressure 

Diastolic pressure + -J- pulse-pressure 

believing that the pressure variations in the aorta are thus more 
nearly portrayed. 

Applying a table originally devised by Beanus, Erlanger and 
Hooker indicate the deductions to be drawn as to cardiac activity 
and vascular resistance from blood-pressure, pulse-pressure, and car- 
diac rate as follows. Since the mean pressure follows the diastolic 
more closely than the systolic they recommend the former as the 
ndicator of blood-pressure in the table. 



Determinable factors. 


Causa tiv 


i factors. 


Diastolic 


Pulse-pressure X pulse rate 
(velocity of flow). 


, Energy from 


Peripheral 


pressure. 


heart. 


resistance. 


Constant 


/ Increased 


Increased 


Diminished 




^ Diminished 
| Unchanged 


Diminished 


Increased 




Increased 


Increased 


Increased . 


• < Increased 


Increased 


Unchanged 




1 Diminished 


Unchanged 


Increased 




| Unchanged 


Diminished 


Diminished 


Diminished 


■ { Increased 


Unchanged 


Diminished 




[ Diminished 


Diminished 


Unchanged 



1 Untersuchungen u. d. Beziehungen zw. Fuellung u. Druck. in d. Aorta, Deutsch. 
Arch. f. klin. Med., 1907, vol. xc. 



168 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

The table, however, is too diagrammatic to be of value except 
as an illustration of the general principles involved. For example, 
cases of nephritic hypertension with increased peripheral resistance 
an d a compensatory increase of cardiac activity show commonly an 
increase both of diastolic pressure and of pulse-pressure X pulse 
rate.. The table would interpret such an effect upon the blood- 
pressure, pulse-pressure and pulse rate as indicating increased car- 
diac activity, hut unchanged peripheral resistance— an entirely 
erroneous interpretation. This limitation in the table is of course 
due to the fact that it deals with changes in the various factors 
only a- to the direction of the change (whether increased or dimin- 
ished), and not as to the degree of the change. 

Widen found that if the two foregoing formulas— Strassburger's 
and that of Krlanger and Hooker— were applied to the same case 
they often led to diametrically opposite conclusions. 

The Energy Index.— Barach 1 found that what he terms the energy 
index (S. 1). R. Index) is useful as a clinical estimation of the 
amount of cardiovascular energy expended, e. g.\ 

Blood-pressure. Pulse rate. I ndex. 

Systolic pressure . . 120 mm. Hg. X 72 = 8.B40 

Diastolic pressure . . 70 " "X 72 = 5.040 

Energy index (sum of 

al)( ; ve) .... 190 " "X 72 = 13.680 mm. Hg. per mm. 

The highest energy index in normal cases is about 20,000 mm. 
Hg. per minute. In pathological cases figures as high as 50,000 were 
encountered. A considerable number of the cases with high indices 
died of apoplexy. 

The Amplitude-frequency Product.— Von Recklinghausen 2 ap- 
proaches the question from a different direction, yet reaches con- 
clusions somewhat similar to those of Strassburger. For him the 
vascular system consists of two reservoirs; the smaller pulsating 
a rterial) and the larger continuously flowing (venous). The circu- 
lation between the two by means of the capillaries is not directly 
affected by cardiac activity. He assumes that to a certain extent 
at Least the diastolic blood flow occurs as in a series of stand-pipes, 
according to Poiseuille's law. He believes that to a certain degree 
the diastolic limb of the pulse wave can be shown to be identical 
with an ordinary outflow curve. He assumes that the arteries 

i The Energy [ndex, Jour. Am. Med. Assn., 191 t, Ixii, 525. 

»Wae wir durch d. Pulsdruckkurve u. d. Pulsdruckamplitude liber .1. grossen 
Kreislauf erfahren, Arch. f. exp. Path. u. Phar., 1906, vol. Ivi. 



THE A \in.l l i DE FREQX ENi I PRODI I / L69 

themselves are not actively concerned in the propulsion of the 

hliiod stream. 1 

Now, if we register the pulse wave Prom a brachial cuff with a 
tambour manometer at a certain pressure, we shall find the curve 
indicating a certain relationship between the amount of blood pro- 
pelled in a given time and the elasticity of the artery. Since it is 
not always feasible to take a tracing and la\ off an absolute sphyg- 
mogram, he suggests as a practical method the amplitude (^pulse- 
pressure) multiplied by frequency (pulse rate) = second volume 
-j- arterial dilatability; in other words, amplitude multiplied by 
raic is proportionate to systolic outpul divided by distensibility. 
Thus, if we can be sure that distensibility remains unchanged, then 
amplitude is a relative measure of systolic output. Bu1 how are 
we to gauge this factor of distensibility? Von Recklinghausen 
suggests that the following axioms may throw some light on the 
question: 

1. With a constant pressure and with increasing tonus the dis- 
tensibility of the artery diminishes. With a decrease of tonus, it 
increases. 

2. Increased arterial tension generally goes hand-in-hand with 
increased vascular tonus. We thus in all probability have a doublj 
decreased distensibility. 

3.' In sclerotic arteries the relative distensibility of bloodvessels 
is diminished. 

We must not use the rules of the blood-pressure quotient too 
absolutely. It is evident that we can draw no mathematically rigid 
conclusions from changes of pulse-pressure even in the same indi- 
vidual, and much less can we hope to use the data thus obtained 
in comparison with other individuals. We cannot by any rule con- 
vert millimeters of pulse-pressure into cubic centimeters of systolic 
output. It has been shown that in the case of the diseased heart 
which is manifesting fatigue, the amplitude-frequency product 
increases less rapidly than in health; it may indeed be entirely lack- 
ing. Tiedemann, who compared the amplitude and the amplitude- 
frequency product in healthy and diseased hearts after the lifting 
of weights, found that in the former case both of these factors 
increased, while in the latter they did so to a lessened extent or not 
at all. These results were indubitable, but what construction should 
be put upon them was less clear. Without a knowledge of the state 
of the vascular tonus no actual figures could be obtained. 

1 This belief has been much questioned of late, based on the observation of Greutz- 
ner that with an equal amount of pressure applied to an artery, more blood can be 
forced out in the direction of normal flow than in the opposite direction. 



17<) FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

Discussion of the Foregoing Tests. — Although not enthusiastic 
over the amount of knowledge to be derived by the use of the fore- 
going tests, I extensively use and place some reliance upon the 
results of Crampton's test. 

Graupner failed to measure pressure before each experiment, 
made his readings too infrequently and allowed the cuff to remain 
inflated too long. This test requires special apparatus. Barringer's 
modification seems to be a distinct improvement. The investiga- 
tions of Swan 1 which concerned themselves with Tigerstedt's, Good- 
man and Howell's, Stone's, and the postural pulse test, led him 
to prefer the first-mentioned two. Pie found that a second phase of 
30 per cent, or less or a cardiac efficiency factor of 40 per cent, 
or over seems to indicate myocardial inefficiency. 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW. 2 

While a knowledge of the state of the blood-pressure is often of 
great value, it gives us no clue as to the rapidity of the circulation 
— the mass movement of the blood. A high vascular tension may 
be associated with a small blood flow and vice versa; for the rapidity 
of the circulation depends not only upon arterial pressure but also 
upon the caliber of the vessels between artery and vein, and under 
some circumstances upon venous pressure. It has been shown 
that the circulation rate increases in proportion to the oxygen 
consumption in a manner corresponding to the increase in total 
ventilation; and it has been suggested that the chief controlling 
factor of the circulation rate is the hydrogen ion concentration of 
the arterial blood. 3 

(i. X. Stewart 1 has devised a method of determining the rate of 
flow which depends on the fact that "the amount of heat produced 
by a part like the hand during rest is negligible in comparison with 
the lieat conveyed to it by the arterial blood. If, then, we deter- 
mine the amount of heat given off by the hand to a calorimeter 
in a given time, and know the temperature of the incoming (arterial) 

1 II'- v% Shall We Tell Whether or Not the Myocardium is Competent, Arch. Int. 
Med., 1915, xv, 269. 
'See i 

3 Boothby, Walter M.: A Determination of the Circulation Kate in Man at Rest 

and at Work, Am. JoUT. Physiol., 1915, xxxvii, 383. 

4 Meaauremenl of the Rate "f Flow of the Blood in Man, Cleveland Med. Jour., 
April, 1911, s, 386; Studies on the Circulation in Man, Heart, October, l'Jll, iii, 33. 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW 171 

and of the outgoing (venous) blood, we can calculate hov* much 
blood must have passed through the band in order that it mighl 
give off this amounl of heat. The quantity of heal given off is 
estimated by putting the hand into a calorimeter. 

"It consists of an inner copper \ esse] containing a know n amounl 
of water (in the experiments usually aboul three liters), into which 
the hand is inserted through an orifice of appropriate size and shape 
in the lid, heat-tigh.1 closure being made l>\ the collar of thick felt 
on the top of the calorimeter. The inner vessel is packed in broken 
cork in a larger outer vessel and the lid is covered with sheet cork 
to reduce so far as possible the loss of heat, and to protect the 
calorimeter against irregular cooling when exposed to draughts. 
The actual loss is estimated by separate control experiments, and 
added to the amount of heat given off by the hand as indicated 
by the rise of temperature in the water. The hand is prepared for 
insertion into the calorimeter by a preliminary immersion I'm' uo1 
less than ten minutes in a large l>ath containing water at approxi- 
mately the same temperature as that in the calorimeter. The 
temperature of the water in the calorimeter is read on a thermom- 
eter permitting hundredths of degrees to be accurately estimated. 
The calorimeter is mounted on a stand which can be raised or low- 
ered by a screw to permit its use either for a patient sitting in 
bed or for an ambulatory patient who is able to sit in a high chair. 
As a general rule the How in the two hands i> simultaneously meas- 
ured. The quantity of blood in grams flowing through the hand 
in the time of the experiment is given by the formula : 



"Here Q is the quantity of blood, // the heat given off by the 
hand, T the temperature of the arterial blood, T 1 the tempera- 
ture of the venous blood, and s the specific heat of blood. In 
estimating H the water equivalent of the hand itself (obtained 
by multiplying its volume by 0.8) and the water equivalent of 
the calorimeter (SO grams) must be added to the quantity of heat 
corresponding to the actually observed rise of temperature. The 
specific heat of blood is taken at 0.9. Knowing the volume of 
the hand, we can express the flow in grams per minute per 100 
c.c. of hand substance. The volume of the hand is easily esti- 
mated by the amount of water which it displaces when immersed 
in a glass douche-can to the level to which it was inserted in the 



172 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

calorimeter. The douche-can is connected by the tubulure to a 
burette, on the scale of which the vertical displacement of the 
water is read off. The amount of water which must be added to 
that in the can in order to give the same level in the burette is 
clearly the volume of the hand. The distance to which the hand 
is to be inserted into the calorimeter is fixed by making a horizontal 
mark with a pencil at the level of the lower border of the styloid 
process of the ulna. A parallel mark is drawn above this at a 
distance equal to the combined thickness of the felt collar and the 
lid of the calorimeter, and this second mark is just kept in view 
above the collar during the experiment. The lower mark must 
then define the limit up to which the hand is enclosed in the calori- 
meter. The collar is supported by a flange around the orifice. 
The temperature of the arterial blood at the wrist is taken as 0.5° 
below the rectal temperature, since this was the difference actu- 
ally found in a normal person. It can be measured by determining 
that temperature of the calorimeter at which the hand neither gains 
nor loses heat. Where the rectal temperature cannot be con- 
veniently obtained the mouth temperature is taken as that of the 
arterial blood at the wrist. The temperature of the venous blood 
is taken as the average temperature of the calorimeter during the 
experiment, since direct estimations of the temperature of blood 
collected by puncture of hand veins, during immersion of the 
hand in baths at known temperatures, showed that the excess of 
the temperature of the venous blood over that of the bath was so 
small as to be negligible for such bath temperatures as are used 
in the experiments." 

The normal average flow as determined by Stewart ranged 
between 3.5 and 1 1 grams of blood per 100 c.c of hand per minute 
at ordinary room temperature, and with an immersion of ten to 
fifteen minutes. Individual variations on different days were more 
or less constant. Elevation of the room temperature increased 
the How. Muscular activity of one hand produced an increase of 
How in that member over its fellow in proportion of nearly three 
to one. Individuals with habitually cold hands exhibited a lower 
rate of How than normal people. A diminished blood flow also 
results from venous stasis produced by moderate constriction of 
the wrist. The local application of heat increases the rate of flow. 

Even a moderate amount of forced breathing decreases blood 
flow, in explanation of which Stewart suggests "acapnia caused by 
the washing out of the carbon dioxide as a possible influence." 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW 17:! 

Mechanical changes in the thorax, and particularly tho e affecting 
the filling and discharge of the heart, musl also be taken into 
account. One moral to be drawn is that while the respiratory 
pump has a part of some consequence in the normal movement of 
the blood, and may even become the preponderant factor when the 
lu-art and the vasomotor mechanisms arc crippled, the idea «•!' the 
"deep-breathing" fanatics thai voluntary interference with the 
delicately regulated respiratory mechanics must be good receives 
no support, at least so far as the circulation in the periphery is 
concerned. 

Further findings regarding the rate of How showed a diminished 
rate in eases of arteriosclerosis of long standing; of brachial neuritis 
with muscular atrophy; and of hemiplegia (associated with com- 
plete abolition of vasomotor reflexes on the affected side). 

An increased flow was found in early peripheral neuritis on the 
affected side, probably owing to a paresis of the vasoconstrictor 
fibers; in a case of occupation neuralgia; in case of an infected 
finger (with partial obliteration of vasomotor reflexes ; in exoph- 
thalmic goitre. 

The Plethysmograph. — This instrument gives us information 
regarding the volume pulse. The volume of all organs varies with 
the different phases of the cardiac cycle with those of the respira- 
tion and with vascular tonus, as well as with certain psychic 
influences, etc. 

The Method. The extremity to be investigated, generally the 
forearm, is introduced into a glass chamber which is filled with 
water and made water-tight by means of a rubber cuff. The water 
contained in the cylinder communicates by means of rubber tubing 
with a recording piston, the upward or downward displacement of 
which imparts its fluctuations to a tambour which records its 
movement on a kymograph. By this means the variations in 
volume may be studied. 

The technic is somewhat complicated, and hence the plethysmo- 
graph is hardly likely ever to become a popular instrument for 
clinical work, but for purposes of scientific investigation, thera- 
peutic effects, etc., it possesses a distinct field of usefulness (Fig. 73). 

The actual amount of blood in the arm can be estimated as sug- 
gested by O. Miiller, 1 by rendering the limb bloodless by immersion 

1 Exper. u. kritische Beitriige zur modernen Kreislauf Diagnostik u. ihr weiterre 
Ausbau durch Einfuhrung des absoluten Plethysmogrammes, Verhandl. d. Kong. f. 
inn. Med., Wiesbaden, 1907, xxiv, 384. 



174 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

in mercury, and then applying an Esmarch bandage to the upper 
arm, the constriction of which is not released until the plethys- 
mography adjustment has been made. The method is not infal- 
lible, however, as the primary anemia tends to the production of 
a secondary hyperemia. Some interesting results were obtained 





4 4k i ' a 


^ c 1 ! 







■ ^ 










iy g^ii,,r rf 


are- 1 






11- ' 1 

■ \ 




■■* v Jttk. ' ^^Jrm" "^^l 


in < -^\gm 


%Jk g^^ffi 




^^i^^B 


H 


Isiill 





•graph: .1, cuff; B, rec< 
D, drum. (After Boffi 



in-; ('. chronograph; 



with the plethysmograph by Weber, who was able to show the 
effecl of psychic stimuli on blood distribution. For instance a 
concentration of attention upon the arm — the subject being told 
in imagine he was performing muscular actions with it — is attended 
by an increased How to t he pan . 



Millions OF ESTIMATING THE RATE OF BLOOD FLOW L75 



Muller has constructed the following table showing the effects 
of different stimuli on blood distribution : 



Hrniii 
Cold + 

Warmth — 

Chloroform + 

Adrenalin + 

1 tesire + 

Disgust — 

Fright + 

Mental effort + 
Sleep ......+ 

Imaginary exercises . . + 



Periphery Abdominal Extremities, 

<>f head. etc. 




Fig. 74. — The finger plethysmograph. (Fleischer.) 



A small finger plethysmograph has been devised by Fleischer. 1 
It must be borne in mind that deductions drawn from plethys- 
mography readings can be applied only to the limb in question, not 
the system as a whole. Particularly useful data may be obtained 
if such observations are made simultaneously with blood-pressure 
observations (Fig. 74). 

The plethysmograph gives us data regarding the peripheral cir- 
culation but tells us nothing as to the underlying causes which 
produce them, as to whether variations are due to an abnormal 

1 Berl. klin. Wchnschr., 1908. 



176 FUNCTIONAL EFFICIENCY OF THE CIRCULATloX 



elasticity, or a small arterial bed, and as to whether these changes 
are normal for the individual or pathological manifestations. How 
greal a part is taken by vasomotor tone, and whether the stimuli 
causing these changes arise in the spinal cord or in the peripheral 
ganglia, or whether the fault lies in the capillaries or veins; upon 
these questions we vainly seek for information. 

A. Mfiller' has suggested that systolic out- 
put might be gauged by the determination of 
the venous pressure. 

The Method. — The circulation in the arm 
is arrested by the sudden inflation of the 
brachial cuff from a large bottle containing 
air under pressure. The venous pressure is 
now measured by the Basch-Recklinghausen 
method, which gives us the resistance (W) 
which the succeeding arterial pressure must 
overcome. The arm is next placed in a 
plethysmograph above which another cuff 
is applied and inflated to about 50 mm. 
Hg., a pressure well below the minimum 
pressure and which therefore does not inter- 
fere with arterial inflow, although it does 
with venous outflow. The pressure in the 
upper cuff is now suddenly dropped to (),. 
the arterial blood flows into the arm but 
cannot flow out of its vein until the venous 
pressure rises above that in the cuff (50 
mm.). Until this occurs the arm is in a 
hydrostatic condition and the resultant 
sphygmographic curve will be a curve of 
arterial outflow (V) (Fig. 75). 

Under these conditions the pressure in the 
occluded region will be a measure of the resistance dl') against 
which the outflowing blood stream operates when the obstruction 
i- removed. The second cuff which measures the venous pressure 
docs not interfere with the inflow but prevents for a time the 
onward flow of venous blood. The height of the first volume pulse 
indicates the value of V. If bodily weight and mean pressure 
arc known, we can calculate I' the systolic output, and I' />, the 

cardiac work. 

i eber Schlagvolumen u. Herzarbeil des Mensehen, I >.-ui <ch Arch. f. klin. Med., 
1909, xevi, 1_'7. 




Fig. 75. -Plethysmo- 
graphic curve used to 
determine Pi I the arterial 
flow into the arm,agains1 
tin- resistance II). 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW 177 

I king this method Muller found thai the systolic outpul averaged 
85 c.c. for men and 25 c.c. for women. An increa ie was found in 
nephritis, cardiovascular disease," exophthalmic goitre, and Addison's 
disease. 

This method has been criticised as theoretically faulty by < Ihristen 
and the practical results have varied considerably from those of 
Plesch. 1 



•svix-, 




Fig. 76. — Hewlett and Van Zwaluwenburg's method for estimating the rate of 
blood flow. Diagram of apparatus for determining the rate of blood Bow through 
the arm. The arm is placed in the plethysmograph /', the opening of which i 
by a piece of rubber dam D, and the connection with the Bkin made tight with 
soapsuds. The narrow pressure cuff C is placed around the arm about 3 cm. above 
the opening into the plethysmograph. The pressure cuff is inflated by opening the 
stopcock connecting it with the large bottle A, in which the pressure has previously 
been raised by the rubber bulb B. Pressures are read by the spring manometer 
M. The plethysmograph is connected with the volume recorder l", which writes 
upon a moving drum. Air can be let out of the system by the stopcock X, and 
water can be introduced from the burette }', so that the writing-point of the volume 
recorder can be adjusted at will. The stopcock 7. serves to disconnect the plethys- 
mograph from the recording apparatus during adjustments of the former. The 
recording apparatus is graduated by allowing 5 c.c. of fluid at a time to flow in 
from the burette, and marking the elevation of the volume recorder thus produced. 



A somewhat similar method of procedure, based on the method 
of Brodie, 2 has been proposed by Hewlett and Van Zwaluwenburg, 3 
to determine the rate of blood flow (Fig. 76). 

The arterial blood enters the organ with undiminished speed at 
first, but soon the flow is retarded by the rise of pressure in the 
veins and capillaries. The organ therefore swells rapidly at first 

1 Hemodynamische Studien, Berlin, 1909. 

2 The Determination of the Rate of Blood Flow Through an Organ, Reported 
at the Seventh International Physiological Congress, August, 1907. (Brodie esti- 
mated the blood flow in an organ by suddenly occluding its peripheral vein and 
measuring the change of volume by means of an oncometer.) 

3 The Rate of Blood Flow in the Arm, Heart, i, 87. 

12 



178 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

and progressively more slowly. The earliest portion of this curve 
represents the rate at which the blood enters under normal condi- 
tions. Brodie has shown that this method gives as reliable results 
as the Stromuhr. 

The following method of testing the circulation time has been 
suggested by Bornstein. 1 The patient is made to breathe C0 2 and 
the time is noted at which the respirations become more forcible. 
This indicates the time taken by the blood to pass through the 
lung and left heart and to reach the respiratory centre; it is assumed 
to be equivalent to half the entire circuit. In health the half- 
circuit is completed in from twelve to sixteen seconds, much less 
time being required after muscular effort, deep breathing and the 
inhalation of nitrite of amyl. 

Fellner 2 believes that the rapid if;/ of flow may be estimated by 
measuring with a stop-watch the length of time required for the 
blood to reach the fingers — travel 50 cm. — after the release of 
tension in a pneumatic cuff applied to an arm previously rendered 
bloodless by bandaging. This method is open to many criticisms. 
( 1 I The air escapes from the cuff too gradually. (2) The vessels 
have been previously emptied and therefore do not offer the natural 
resistance to the flow. (3) The blood path from the brachial to 
the digital arteries is not direct, owing to the branching and steady 
diminution in caliber of the arterial tree. 

The Krogh-Lindhard Method. — "The principle involved is, briefly, 
to determine the rate of absorption of nitrous oxide in the lungs. 
Since nitrous oxide is a readily soluble gas, yet one which forms no 
chemical combination with hemoglobin, it will go into solution at 
body temperature according to a definite coefficient. This coeffi- 
cient has been determined by Siebeck. This being true, if, after 
having breathed a mixture of air and nitrous oxide, the subject 
bolds his breath for a certain length of time, and we then deter- 
mine the percentage of nitrous oxide in the alveolar air at the begin- 
ning and at the end of this period, together with the total amount 
of gas enclosed in the chest during the period of holding the breath, 
\\c can calculate how much blood must have passed through the 
lungs to remove the amount of nitrous oxide which has disap- 
peared." 8 

1 Eine klinische Methode /.. Schatzung d. Kreislaufzeit, Miinchen. med. Wchnschh, 
l'.U-.', lix, l isc. 

1 Daa Pulsometer, eia prakt. [nstrumenl ■/.. Beatimmung d. Stromgeschwindig- 
keit dee Blutes am Lebenden Menschen, Deutsch. med. Wchnschr., 1907, No. 15. 
Means, J. H., ami Newburgh, L. II.: Studies of the Blood Flow by the Method 
of Krogh and Lindhard, Tr. Ass,,. Am. Phys., L915, \\\, 51. 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW 17!) 

A modification of this method has I ><<•( i devised bj Means and 
New burgh, which consist of: 

1. The oxygen absorption (this, . . . was done by a short 
experiment \\ iih the 1 >ouglas bag). 

2. The hemoglobin and consequently the oxygen capacity (bj 
the fjellige colorimeter . . . i. 

.'!. The percentage saturation of the venous blood with oxygen. 

4. The pulse rate. 

"The thiol determination, that of the percentage saturation of 
tin' venous Mood with oxygen, is obtained l>y withdrawing a 
sample of blood from an arm vein into a syringe containing a little 
potassium oxalate solution, and from which all air bubbles have 
been expelled. (We also found it well to grease the plunger of the 
syringe.) From this syringe the blood was directlj introduced 
beneath the ammonia solution in one of the bottles of tin- Barcroft 
differentia] blood-gas apparatus, without being exposed at an> time 
to the aii-. Its percentage saturation with oxygen was thereupon 
determined. 

"Having obtained these factors we proceeded to calculate the 
blood How. In the light of Barcroft's determinations of the oxygen 
content of arterial blood, we have assumed thai the blood leaves 
the lungs 94 per cent, saturated. If then the percentage saturation 
of the venous blood is found to be 60 per cent, the coefficient of 
utilization of the oxygen capacity will be the difference between 
the two, or 34 per cent. Knowing the oxygen absorption, the 
coefficient of utilization, and the oxygen capacity, we calculate 
the blood flow from the formula : 

Blood flow per minute = 0: ^sorption per minute 

(coefficient) (oxygen capacity) 

and the volume per beat: 

, r , , Blood flow per minute 

\ olume per beat = — 

Pulse rate 

The accuracy of the method depends entirely upon whether the 
percentage saturation of the blood in the arm vein is any criterion 
of that in the right heart. At the present time we are unable to 
say positively whether this is true, and consequently only propose 
this method tentatively. ^Ye believe, however, that it is a fair cri- 
terion, and base this belief in part upon two animal experiments 
in which we took samples of venous blood from different localities 
and found a fairly close percentage saturation in the different 
samples." 



180 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

Using this method the last-named authors found in two normal 
subjects a rest flow of 4 to -H liters per minute. In response to 
increasing amounts of work the blood flow rose to 15 litres per 
minute. 

The Tachograph. — The blood Jlcnv in the arm may also be esti- 
mated by means of a sensitive flame. Von Kries's instrument, 
devised for this purpose, is known as the tachograph. 1 "The fore- 
arm is inserted into an air-tight glass cylinder, but in this case no 
water is introduced. With each systole of the heart a certain 
amount of air is forced out of the cylinder through the rubber 
tubing into a specially devised gasoline burner. The expelled air 
causes the gasoline flame to flare upward to a height proportional 
to the amount of air displaced. This flame is in turn photographed 
upon a revolving strip of paper sensitized with bromide of silver. 
When the tracing is developed it presents a succession of zigzags 
at first glance resembling the results of the electrocardiogram" 
(Fig. 77). 

When the arm increases in volume during the ventricular systole, 
the enclosed air, meeting with no resistance to outflow through 
the tubing will emerge the more rapidly and suddenly the more 
quickly the blood is forced into the arm (Figs. 78, 79 and 80). 

The Estimation of Resistance in the Large Vessels. — Bracking 2 
made brachial blood-pressure observations in the following postures: 
A, recumbent; B, sitting in bed with the legs extended; C, sitting 
with the legs dependent; I), standing. 

Normally, the pressure is highest in B, which he explains as 
due to a compensatory peripheral contraction instituted to prevent 
splanchnic anemia. It is further increased by pressing the legs 
against the abdomen. If there be circulatory weakness, the maxi- 
mum pressure in B is lower than in A, showing a loss of peripheral 
arterial power. 

The Estimation of Arterial Functionation. — O. Miiller employs the 
following method: The arm is introduced into a plethysmograph 
and ice is applied to the arm above the instrument. Normal arteries 
show a distinct diminution, and, upon withdrawal of the cold, an 
increase in volume. In sclerotic arteries these changes are in part 
or entirely lacking. This test, although for the most part corrobo- 
rated by other investigators has also been criticised. 

1 Ein Neues Verfahren zur Beobac-htung der Wellenbewegung des Blutes, Berl. 
klin. Wchnachr., 1887, p. 589. 

2 Ein Beitr&g zur Funktionsprfifung der Arterien, Ztechr. f. exp. Path. u. Therap., 
1907, iv, Pt. I. 




-Central tachogram, reading from right to left: 
exercise. (Muller and Veiel.) 



at rest; b, after 




Fig. SO.- 



central tachogram in aortic insufficiency; b, peripheral tachogram in 
aortic obstruction. 



182 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

Cold contracts and beat dilates the arteries of healthy people 
hut the psychic state also plays a considerable part. It is therefore 
accessary to arrange plethysmography examinations in such a 
manner that thermic and psychic influences shall not be separated. 
EveE if after repeated trials the vessels do not react one cannot on 
that account diagnosticate an anatomical lesion. One cannot con- 
clude that a man is arteriosclerotic because his vessels do not react 
to ice, because many organic cardiac maladies do not give this 
response, but merely that his arterial fnnctionation is not normal. 
In the majority of individuals hardened arteries are hyporeactional, 
in- even areactiona] to ice, although some of them are hyper- 
reactional. 1 




Fig. 81. — A. kymograph; B, plethysmograph of Mosso; B', plethysmograph of 
Wiersma; C, cuff; D, manometer; E, pump; F, escapement; a, tambour with pen; 
'-. escapement; c, occlusive rubber cuff; d, stopcock; e, three-way glass tubing. 



The Estimation of Vascular Tonus. — De Yries-Reilingh 2 suggests 
the following method for determining the degree of arterial tonus: 

A small cuff is applied to the arm while the forearm is placed 
in a plethysmograph. Pressure is suddenly raised above the systolic 
presgure in the upper cuff. The tambour of the plethysmograph 
now registers a straight line; but as soon as pressure in the cuff 
falls sufficiently to allow blood to pass through, the tambour will 
rise. The pressure at this point is the maximum arterial pressure 
plus the arterial tonus. If pressure is gradually lowered a further 
rise of the tambour due to venous stagnation will occur. Hut in 
time a point will be reached at which the tambour falls because 
the cuff pressure has become less than the venous pressure. The 
difference in pressure between the first elevation and the first fall 
of the tambour is taken as the index of vascular resistance. This 
factor was found to range between 17 and 32 mm. Ilg., the normal 
average being L8 mm. A source of error lies in the fact that during 



[Jeber d. Bedeutung u. Technik d. Plethysphyg- 
gesunder u. kranken Arterien, Ztschr. f. klin. 



1 Romberg, IV, and Miiller, < ». 
mographischen Funktionspriifun 
Med., L912, Ixxv, 92. 

«Zur Blutdruck -sunt;, Ztschr. f. klin. Med., 1913, lxxvii, 0' 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW 183 

this prolonged procedure for some reason a general increi 
pressure occurs. This rise of pressure renders an estimation of the 
minima] pressure unreliable, and while such a rise may be ob\ iated 
by placing the cuff at the distal cud of the Forearm, a new source 
of error is thus introduced by the protected position of the arteries 
at this point. The results would probably also vary according to 
the rate at which the cull' pressure was lowered (Fig. 81 . 

The Diastolic Index. It has been suggested thai some light might 
be thrown upon vasomotor responses by observing the diastolic 
pressure as recorded while manometric pressure i- being L) 
increased, (2) decreased. Macwilliam and Melvin 1 found that 
different readings (20 mm. I [g. i arc somel imes thus obtained. The' 
construe this phenomenon, which is a rarity, as a result of sluggish 
vasomotor response to obliteration of a large arterial branch. It 
occurs more frequently if simultaneous readings are made on both 
arms. 

The Estimation of Capillary Blood-pressure. Various and for the 
most part unsatisfactory methods of measuring capillar} pressure 
have been suggested see page III. \W have had no persona] 
experience with the determination of the capillar} tension, hut it is 
manifest that if a method can be devised which i- both accurate 
and clinically applicable much valuable information will he 
obtained. Simultaneous observations on the relationship between 
the arterial and the venous pressures yield more important data 
regarding the state of the circulation than either alone, since the 
arterial represents the beginning and the venous the end of the 
greater circulation. 

Combined Observations. — A more accurate though clinically inap- 
plicable method of functional diagnosis originally described by 
Marey and lately rejuvenated by (). M filler, Romberg, and F. 
Kraus, consists of: 

1. Prolonged continuous observation of the systolic and diastolic 
pressures. 

2. Continuous tachographic observation undertaken simultane- 
ously with the foregoing. 

If both pressure and rate increase it is assumed that we are 
dealing with an increased systolic output; if the two values move 
in opposite directions, that an alteration of peripheral resistance in 
the arm under observation has occurred. 

3. Plethysmographic observations to determine vascular changes 
in the arm. 

1 Some Observations on the Significance of Blood-pressure Readings in Man, 
British Med. Jour., November 7, 1914, p. 2818. 



Is! FUNCTIONAL EFFICIENCY OF THE CIRCULATIOX 

But even this method does not permit us to draw deductions 
which can be expressed in actual figures. 

The Sphygmobolometer. — This instrument, devised by Sahli, 1 is 
used to estimate the energy of individual jtul.se waves, and thus 

indirectly the energy of cardiac systole. 




Fig. 82. — Schematic diagram of Sahli's sphygmobolometer: A, cuff; b, inflating 
bulb; C, mercurial manometer; E, graduated piston pump; </, index manometer. 
Lower diagrams: .1 , lateral view of the steel cuff; E, index manometer in horizontal 
and eivrt position. 

The Principle.- The pulse wave is made to transmit its force to 
a measured quantity of air enclosed in a cuff (A) encircling the 
forearm and communicating with a manometer. The pressure 

in the cuff is raised until the maximum oscillation occurs in the 
oscillator u/), this point being known as the optimum pressure. 



1 Sahli's Diagnostic Methods, 1911, p. 186. 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW LS5 

This is accomplished through the use of a steel outer cuff, with 
which tension can be very exactlj regulated and the precise point 
noted at which the maximum oscillation is overstepped. 

The energy of thai portion of the aortic wave which reache the 
brachial artery is expended in three direction-: (1) Thai which 
passes the cuff. (2) That which is reflected backward toward the 
heart. (3) That which compresses the cuff. Manifestly only the 
latter portion can be measured, thus ever leaving two undetermin- 
able factors. 

By observing the actual height of the manometric pressure which 
corresponds to the optimum pressure, l>\ noting the extent of 
oscillation of the latter, and knowing the volume of the enclosed 
air, we are enabled to construct a formula which represents the 
amount of energy expended. The volume of air is measured l>\ 
means of a graduated piston syringe i /.' with a capacity of 200 c.c. 
The cubic capacity of the index manometer is determined for each 
individual instrument, the lumen being calibrated in such a manner 
that each centimeter of length is equivalent to 0.02 c.c. The instru- 
ment is based upon Boyle's (Mariotte's) law that if temperature 
remains constant the volume of gas will vary inversely as the 
pressure, whence follows the formula: 

w = y W) (ftpW 13 - 6 

11" = work performed by each pulse wave. 
V = volume of air. 
(A p) — maximum oscillation reduced to cm. II . 

B = mean barometric pressure = 76.4 (New York). 

P — pressure in cm. Hg. at maximum excursion of index manometer. 



\B + P/ 


\B + PJ 


P. 


V. 


5 


0.78 


6 


0.92 


7 


1.04 


8 


1.16 


9 


1.28 


10 


1.39 


11 


1.49 


12 


1.59 


13 


1.69 


14 


1.78 


15 


1.S7 


16 


1.95 


17 


2.02 


18 


2.10 


19 


2.17 


20 


2.23 


21 


2.30 


22 


2.36 


23 


2.42 



A table can be worked out so that each estimation requires but 
one multiplication: (A p) X (F X V). 



186 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

The accuracy of any single determination depends mainly on 

the leading of (A y/), errors in the other terms being negligible in 
comparison. This involves a reading of the excursions of the kero- 
sene index and a calibration of these excursions in terms of mer- 
cury. Computations show that under normal conditions results 
obtained by an experienced observer can be relied on to better 
than 10 per cent. (Potter). 1 




Fig. 83. — The sphygmobolometer. The rubber bag D is applied over the radial 
artery by the cuff // and connects by means of tubing with the (1) 10 c.c. syringe 
G and (2) with the index manometer E, F, which contains colored kerosene and 
(3) with the vertical manometer A. (Sahli.) 



"The value of 7i in a given locality may be assumed to be con- 
stant, as may also the volume V for a given instrument. A similar 
table would have to be worked out for each individual instrument. 
W = F x V x (A p) 

"The total work of the pulse per minute is obtained by multiply- 
ing the work of a single beat by the pulse rate. We are of course 
ma measuring the entire energy of the heart but only that fraction 
of it which is consumed in furnishing the pulse wave in the brachial 
cuff — this Sahli believes to be a constant fraction. "- 

'.lour. Am. Med. Assn., April L9, 1913, p. 1211. 

- For more detailed discussion sec Sahli: Deutsch. med. Wchnschr., 1907, No. 16, 
p. 628; No. 17, p. 665. Sahli: Diagnostic Methods, edited by Potter, W. B. Saun- 
ders Company, Philadelphia, 2d ed. Sahli: Deutsch. med. Wchnschr., 1910, No. 
17, p. 2181. Christen: Ztschr. f. klin. Med., 1910, Ixxi, 390. Sahli: Ztschr. f. 
klin. Med., 1911, lxxii, 1. Sahli: Ztschr. f. klin. Med., 1911, lxxii, 214. Christen: 
Ztschr. f. klin. Med., 1911, lxxiii, 55. Christen: Deutsch. med. Wchnschr., 1911, 
No.l4,p.644. Christen: Cor.-Bl. f. schweiz. Aerzte, 1911, p. 562. Sahli: Ztschr. 
f. klin. Med., 1912, Ixxiv, 230. Christen Ztschr. f. klin. Med., 1912, Lxxiv, 117. 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW 187 

The most recent modification of sphygraobolometry 1 con i 
the substitution of a Jacquet sphygmograph equipped with a spiral 
spring in place of a pneumatic cull'. The coefficienl of elasticity 
of the spring is practically constant for different pressures, hence 
it is possible to take the arithmetic mean of the beginning and 
end tension of the pressure. In order to translate the spring ten- 
sion into grams the apparatus is equipped with a device to 'haw 
upon the smoked paper nine parallel al>seissa\ For each of these 
abscissse, the pressure value of tin- spring is established in grams 
and tabulated. These abscissas indicate the heighl of the pelotte 
phis the magnification due in the tambour. Thus it i~- possible to 
take tracings of differenl degrees of spring pressure, choosing those 
as our criteria which yield the largest work product. Needless to 
say, a sphygmograph must he applied with accuracy and care. 

Dynamic Diagrams. T. F. Christen suggests the use of "dynamic 
diagrams" 2 as an index of cardiac work, a conception which he 
bases on the following hypothesis: 

The Theory. The old-fashioned palpation of the pulse tells us 
much more about the condition of the circulation than does the 
sphygmogram, in spite of the hitter's seemingly higher scientific 
character. In the clinical sphygmogram there i- no exact relation 
between the ordinates and the pressures. We do not even know- 
where to trace the level of the pressure zero. Even if there were 
such a relation, sphygmography would --till not be a dynamic 
method, as in dynamics we do not ha\ e to study alone the temporal 
variations of the forces, but essentially the effect of these forces. 
These two statements sufficiently explain the failure of the clinical 
sphygmogram. There are two dynamic diagrams of the pulse that 
may be determined in a mathematically exact manner. They are 
the graphic expression of clinical experiments based upon the fol- 
lowing two questions: (a) What is the systolic increase of volume of 
the arteries covered by a pneumatic cuff by a given pressure? (b) 
What is the amount of mechanical energy required for this move- 
ment? These dynamic diagrams, called stasis curves, are charac- 
teristic of the behavior of the pulse against a stasis pressure. They 
depend on the volume of air within the cuff as little as they do on 
the elasticity of the cuff and the soft parts. They depend only on 
the breadth of the cuff. We therefore have to compare stasis 

1 Lipowetsky, L. : Sphygmobolometrische Untersuchungen an Gesunden und 
Kranken mittels des Sahlischen spkygmobolographischen Verfahrens, Deutsch. 
Areh. f. klin. Med., 1913, cix, S. 498-514. 

2 Die neuen Methoden d. Dynamischen Pulsdiagnostik, Ztschr. f. klin. Med., 1911, 
lxxviii, 55. 



Iss FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

curves derived from experiments with cull's of the same breadth. 
The exclusive consideration of pressure and its temporal variations 
will never permit us to solve the question of diagnosis of the pulse, 

for the mechanics of the pulse contain essentially dynamic prob- 
lems more than any other province of physiology. The stasis 
curves (dynamic diagrams) replace the palpation of the pulse by 
an exact method, because they answer the same questions that 
palpation does, informing us concerning the "filling" and the 
"intensity" of the pulse. The method depends on the estimation 
of the force necessary to produce the oscillations which are observed 
in the determination of the pulse-pressure. This variation in the 
volume of the artery does not depend on the volume of air within 
the cuff, nor on the elasticity of the system. It can depend only 
on pressure exerted by the inflated cuff and on the dynamic 
qualities of the pulse. 

The Method. — In order to find the value of the systolic increase 
of volume, i. e., the volume of blood the pushing forth of which 
against the pressure of the cuff produces the oscillations observed 
on the manometer, we make use of a syringe whose piston has to 
be pushed in up to the point where the oscillations have been 
displaced about once their own amplitude. 

Example. — We observe on the manometer oscillations between 

(gr. 
The unit of the manometer is 
cm. 2 

Pushing in the piston of the syringe we increase the pressure within 

the cuff, elevating both limits of these oscillations. We do this in 

such a manner as just to reach the point where 176 has become 

the lower limit of the oscillations, having been heretofore its upper 

limit. Thus we are sure that the volume of the piston, which is 

read off on its own scale, must be that incompressible volume 

which brought under the cuff increases the pressure within it from 

170 to 176. Two incompressible volumes, which, forced into the 

same air-chamber produce the same increase of pressure within it, 

must be equal. Therefore the volume read off and the piston 

must be equal to the systolic increase of volume of the artery (or 

mi cries) that is covered by the inflated cuff. Suppose that we read 

a volume of 0.7 cm. 3 , then the mechanical energy required for the 

same increase of volume — the main pressure being: 

17:5 -- - must have the value L73 — X 0.7 cm. 3 = 121 gr. cm. 
cm. 2 cm.- 

In this way we find for every pressure (P) a volume (V) and an 
energy (22), the relation between which is E = PV. Repeating 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW L89 

this experimenl at different pressures we get a series of pres ure 
volumes and energies which we arrange in the following manner: 



Pressure. 
80 
120 
mi 
L65 
190 
210 
225 
240 
250 



Ex \mim.i: 

Volume. 
0.1 
0.3 

1 1 , :,:, 

0.9 

1.2 

1.2 

0.9 

0.4 

0.2 



Energy. 

8 
36 

77 
1 l'.i 
228 
252 

i'ik; 
>u; 
50 

















\r-^~* K ^ -^ 


a < 


TB^^t 




k V 




\ I 




x_ _\ v 


- 


X 


15 t 


£L X \ 


1.5 / 


/ ' -H^- ^ 


J 




7 - ^ 




t 7t 


n r 




i 1 


1- 4 - 




t -/ -*C 




t 7 <S\ 


— v— 




- C 


/ - ' ? ■' 


4 


X- ?^jf- \ 


-L 




\ 


-+**^<? ^fc 


V 


5^2 ir _£ _ 









l-'O 



L50 



•.v.i 



300 



35ft 



Fig. 84. — Dynamic diagrams. Curve of volume: 1, that of health; 2, of myo- 
carditis; 3, of aortic insufficiency; 4, of arteriosclerosis. In cases of forcible pulsa- 
tion — arteriosclerosis, aortic insufficiency — the volumes may exceed 2 cm. and the 
energy 600 gr. cm. Furthermore, the character of the summit is quite different 
from that of arteriosclerosis. 



Diagrams. — In order to give a clearer idea of the relation between 
these quantities, viz., pressures, volume, and energy, we plot two 
curves which represent the volumes or the energies as functions 
of the pressure. Therefore in our graphic method we have to plot 
the pressure as abscissa? and the volumes or the energies as ordi- 
nates. The author employed the leg instead of the arm for these 
determinations, because he found that in cases of hypertension 
disagreeable sensations and even pain may be produced, an occur- 



190 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

rence which it is said can be avoided when the cuff is fastened 
anmnd the calf < Fig. 84 \. 

We have had qo experience with Christen's method. The author 
claims that the results obtained by it when applied in studying 
the effect of work, rest, medication, etc., are satisfactory. It is 
essential that the variations of the summit -a rise or a fall, a 




Fig. 85. — Christen's energometer. 



shifting to a higher or lower level, a sharpening or flattening of 

the curve (Fig. 84) — be expresssed in absolute values, the pressure 

gr. 
in — , the volume in cm. 3 and the energy in gr. cm. 1 
cm. 2 

Extreme care in technic is absolutely essential. The readings 
musl !><• taken with the patient as well as the patient's arm in the 
same position. The cuff must be applied to exactly the same region 
of the arm, which should be marked, and needless to say the same 
arm must be used for successive observations (Dunkan). Leg read- 
ings arc inaccurate. The energy of the pulse wave even in normal 
subjects is variable, but there are limits which are not normally 
exceeded. Muscular exercise, and cardiac hypertrophy with good 



1 ( 'lirisicn's energometer, 
Bt ( iallen, Switzerland. 



tufactured by Hausmann Instrument Company 



METHODS OF ESTIMATING THE RATE OF BLOOD FLOW I'M 

compensation show high readings. Adrenalin injections cause high 
values independently of any effect on blood-pressure (Drouven). 
The Determination of Intra-abdominal Pressure. Blood-pressure 
may be considerably influenced by intra-abdominal pressure, on 
which account it is sometimes desirable to know what the height 
of the latter pressure is. This may be determined I , as sug 
by Moritz, by introducing into the stomach a tube into which a 
thin rubber window has been inserted, the tube being connected 
with ;i manometer. (2) By means of a special instrument devised 
by Engelen 1 which consists of a large glass bell, the bottom of which 
is scaled with a thin rubber dam. The latter will project either 
inward or outward, as the pressure relations on either side of the 
membrane may vary. 




Fig. 86. — Engelen' s instrumenl for the determination of intra -a In luminal pressure. 

The instrument is placed upon the abdominal wall, connected 
with a manometer, and sufficient air is pumped into the hell to 
equalize the pressure on each side of the membrane in the interior 
of the bell and the outer abdominal wall — this being shown by an 
indicator. 

Deep inspiration may cause a pressure of —57 mm. Hg.; forced 
expiration, +87 mm. During normal parturition a pressure of 40 
mm. is usual which with dystocia may rise as high as +125 mm. 

(3) Variations in abdominal pressure may also be determined by 
inserting a rubber bag (cylinder in casts 7 cm. by 16 cm.) into the 
rectum, which when inflated with air is connected with a Marey 
tambour.' 2 The normal intra-abdominal pressure is above that of 



1 Ueber Messung u. Bedeutung des Abdominaldruckes, Deutsch. med. Wchnschr., 
1911, No. 19. 

2 Weber, E. : Ueber eine neue Methode zur Untersuehung der Druckschwank- 
ungen in der Bauch Hohle, Zentralbl. f. Physiol., Leipsic u. Wien, 1906, xx, 329-336. 



192 FUNCTIONAL EFFICIENCY OF THE CIRCULATION 

the atmospheric pressure. It fluctuates with the respiratory excur- 
sions of the thorax and the diaphragm. Anything which dimin- 
ishes the tone of these structures causes a lowering of abdominal 
pressure. Distention of the abdomen by fluid or gas increases the 
pressure and this is in turn followed by a fall of blood-pressure due 
to a diminished venous inflow, and consequently a decreased left 
ventricular systolic output 1 (see page 44). 

1 Emerson, H.: Intra-abdominal Pressure, Arch. Int. Med., 1911, vii, 354. 



CHAPTER VI. 

AJRTERIAL HYPOTENSION. 

ESSENTIAL HYPOTENSION (CONSTITUTIONAL LOW 
ARTERIAL PRESSURE). 

Arterial hypotension, by which we understand a systolic 
pressure of or below 115 mm. Fig., generally in association with a 
diastolic pressure below- 80 mm., is a very common condition. 
Hypotension may occur after hemorrhage, in acute infectious dis- 
eases, in conditions of malnutrition or cachexia, such as tubercu- 
losis, carcinoma, Addison's disease. It may also occur in anemia, 
in paresis, in osteo-arthritis, in cardiac dilatation, tachycardia and 
in cardiac decompensation. Hypotension is also noted in associa- 
tion with abnormalities of the endocrine functions of the male 
gonads, and in certain individuals who, although apparently healthy 
are not robust, in whom it appears as part of their constitutional 
makeup. Two renal conditions cyclic and orthostatic albumin- 
uria, and amyloid disease of the kidney are often associated with 
low blood-pressure. It may also occur as a result of intoxication— 
anaphylaxis, nicotinism, alcoholism. Hypotension also occurs in 
surgical shock; as a result of some forms of anesthesia, especially 
that of chloroform, and as a terminal event during the last ebbing 
tide of life. 

Relative hypotension often follows hypertension when vascular 
and cardiac resources are overtaxed. 

Symptomatology. — Essential hypotension is a very common con- 
dition, the importance of which has been signally emphasized by 
L. F. Bishop. Many apparently healthy individuals, although not 
robust, often in youth and early adult life normally have a systolic 
and a diastolic blood-pressure ranging between 115 and 100, and 
between 80 and 70 mm. respectively. Such individuals lack stamina, 
tire easily, complain of cold extremities and of the inability 
to do prolonged mental or physical work. They often suffer 
from dyspepsia, which upon investigation proves to be of the 
"nervous" variety, not infrequently due to hypomotility and super- 
imposed on an anatomical background of partial or total splanch- 
13 



194 .1 RTERIAL If YPOTENSION 

noptosis. They are not actually ill, yet they are rarely well; they 
complain of all sorts of symptoms, headache, lassitude, mental 
depression, "gouty" pains, constipation, etc. Their bodily temper- 
ature is generally subnormal in the morning and they suffer from 
cold extremities due to a sluggish peripheral circulation. They are 
apt to be filed away in that much overloaded diagnostic pigeon- 
hole labeled "neurasthenia." They are often of the high-strung 
nervous temperament, "go on their nerves," are moody and emo- 
tional, and sensitive to caffein and nicotine, as well as to atmos- 
pheric and barometric fluctuations. Staehelin 1 found that a fall of 
barometric pressure produces a lowering of the arterial tension in 
many individuals. In extreme cases they often fall asleep when 
sitting upright and suffer from insomnia when they go to bed. 
Perhaps enough has been said to illustrate the picture, although 
pages might be written upon the symptomatology. 

The inability of the subjects of constitutional hypotension to 
stand the demands of prolonged physical exertion is the direct 
result of their low blood-pressure. Recent experimental evidence 
has shown that an increased arterial pressure such as occurs nor- 
mally during exercise increases the height of muscular contraction 
when the pressure is below a certain critical level, whereas a 
decreased pressure below this point has the opposite effect. An 
increased flow flushes out and neutralizes the fatigue products. 2 

Observations over a period of two years in a case of constitutional 
low tension by Edgecombe 3 showed that pressure was higher in 
the evenings than in the mornings. No relationship could be estab- 
lished between pressure and pulse rate. Exercise, mental effort, 
grief, altitude, tea, coffee, and tobacco had a pressure-increasing 
effect. Constipation lowered the tension. Therapeutically, caffein 
and pituitary substance raised, whereas alcohol lowered the pressure. 
Strychnin, digitalis, calcium, and glycogen were without effect. 

While it is unsafe to generalize from a single case, the results 
reported correspond quite closely to what is usually observed in 
this class of eases. 

Patients with essential hypotension not only have an habitually 
low blood-pressure, but their response to different stimuli which 
normally affect blood-pressure either locally or generally is either 
quantitatively or qualitatively abnormal. The effect of a change 

i eber '1. Einfluss d. fcaglichen Luftdruckschwankungen auf den Blutdruck, Med. 
Klinik, 1913, ix, SOL'. 
'•' < '.ruliiT, ( '. M.: Studies in Fatigue, km. Jour. Physiol., 1913, xxxii, 221. 
i Soc. Med., Med. Sect., February 28, L91 L. 



ESSEh II I/. HYPOTENSIOh L95 

of posture from the recumbent to the erecl po ition is normally a 
variable one, but the maximum and minimum pressures invariably 
approach each other (Erlanger). The pulse rate decreases, the 
pulse-pressure Tails. These changes are due to the effect of gravity. 
The pressure in the femoral artery is higher than thai in the carotid 
in proportion to the difference of the hydrostatic pressure of the 
column of blood which separates the two points of measurement. 





















column separating 


Posture. 


Brachial. 


Tibial. 




artnli 


Horizontal 


. I 10 


138 


2 





Standing 


L36 


204 


68 


68.5 


1.. [misI .. Ic^s up . 


. 122 


7(1 


16 


16. 1 


Vertical, head down . i 18 


Til 


7s 


77 .7 



If norma] postural change in pulse rate (6 to 10 beats) 'I'" no1 
occur, it shows too much; if exaggerated, too little splanchnic 
tone. If the response is reversed there is apt to be extensive dis- 
ease of the cardiovascular system generally hypertension. In 
healthy individuals the transition from the recumbenl to the ered 
posture generally produces a slight fall of the systolic and a rise 
of diastolic pressure, thus a diminution of pulse-pressure. In people 
with relaxed abdominal walls and enteroptosis a marked falling 
of the systolic pressure (25 nun i and a slight lowering of the 
diastolic pressure have been noted. 1 (See Crampton's test, p. L52.) 
A lowered splanchnic tone leads to more or less cerebral anemia, 
and a sudden assumption of the erect posture when the individual 
has been recumbent or stooping to the ground with the knees 
Hexed often causes a temporary vertigo. Syncopal attacks from 
relatively insufficient causes are in ease of the female sex. at least, 
by no means rare. An engorged condition of the viscera is often 
evident on inspection during abdominal operations. The vascular 
supply especially in the veins is excessive. Ptosis of the right 
kidney not only tends to constrict its own vascular supply, but by 
dragging upon the inferior vena cava and the aorta may seriously 
disturb the lumen of these vessels, contributing in no small measure 
to vascular stasis. 2 These results are noted clinically by the large 
gush of urine which often follows a short period of recumbency. 
(See Arterial Functionation, p. ISO.) 

Another frequent symptom resulting from low blood-pressure is 

1 Birtch, Fayette W., and Inman, Thomas G. : Blood-pressure Observations on 
Patients with Relaxed Abdominal Musculature, Jour. Am. Med. Assn., 1912, lviii. 
S. 265-268. 

2 Mackenzie, K. A. J.: The Role of Movable Kidney in Intestinal and Vascular 
Stasis, Jour. Am. Med. Assn., 1912, lix, 338. 



196 ARTERIAL HYPOTENSION 

headache, relief from which is too often sought in headache pow- 
ders, which of course eventually aggravate the condition. Eleva- 
tion of blood-pressure is followed by improvement. 

Etiology. — "In the upright posture the blood tends to settle 
in the capacious channels of the splanchnic vascular bed. The 
'head-up' position in four-footed animals may lead to extraordinary 
lowering of blood-pressure in the carotid arteries and presumably 
to critical anemia of the brain. But in man there has been devel- 
oped a compensatory reaction, undoubtedly chiefly vasomotor, by 
means of which the vessels of the dependent parts of the body, 
probably the arteries of the splanchnic area, contract under stimulus 
of the upright posture and maintain a fairly uniform distribution 
of the blood mass. 

"The splanchnic and the systemic veins are capable, when dilated, 
of containing a large proportion of the total volume of the blood. 
Under exercise the blood which is in excess of the amount which the 
heart can handle, is stored in the systemic veins. During rest this 
blood is again reservoired in the splanchnic veins. The normal 
give and take balance between these two storage depots may be 
upset. In the hypotensive cases the splanchnic vessels remain over- 
loaded, too little blood reaches the heart, the systolic output is 
small and arterial tension low. The opposite condition obtains in 
arterial hypertension. 1 (See Abdominal Pressure.) 

"No physiological coordination can be conceived that is more 
important than this to the welfare of the organism as a whole. 
It is to be expected, therefore, on a priori grounds, that minor 
compensations having the same general purpose should here and 
there disclose themselves. When the radial pulse fails in a wrist 
which is raised above the level of the head, the result may be due 
either to passive drainage of the blood from the artery, followed 
by a purely local contraction of the arterial wall, or to active vaso- 
motor contraction of the vessel under the stimulus of gravity. As 
touching the former view, Bayliss has shown that peripheral 
arteries freed from their nervous connections respond to variations 
of internal pressure by contracting as the pressure rises and dilating 
as it falls. Sifting the great number of observations bearing on 
this subject, the latter explanation seems to be the only possible 
one. In other words, according to this view pulse failure in the 
elevated radial artery is a sign of vasomotor activity and belongs 
to the series of physiological compensations. It is comprehensible 

1 Hill, Leonard: [nfluence of the Force of Gravity on the Circulation of the Blood, 
Jour. Physiol., Is'.).",, xviii, 1.3. 



ESSENTIAL 11 V 1'OTENSION 197 

as such, if we presume thai contraction of the radial arteries helps 
to maintain blood-pressure in more vital tissues by diverting the 
bloodstream from less sensitive organs, h has often been observed 
that pulse failure which is obvious in the elevated wrisl at the 
beginning of a series of observations is not evidenl later on. That 
is, the pulse failure mechanism seems subject to fatigue. Excite- 
ment or emotion which increases the total outflow of nerve energy 
tends to inhibit the pulse failure. In general, in perfecth normal 
individuals who are in vigorous physical condition, the radial pulse 
is maintained when the arms are raised. In the same class of per- 
sons, when more or less debilitated by confining occupations or 
subnutrition, the pulse often fails. In an acute febrile disorder the 
pulse usually remains when the arms are raised; during convales- 
cence, especially with the establishment of compensal ion in cardiac 
disease, the pulse often fails. Numerous observations seem to -how 
that these differences in the reaction of the pulse do not depend on 
the amount of blood volume or the degree of maximal arterial 
pressure. It is not only conceivable, but probable, that signs of 
physiological compensation which are absent during robusl health 
or active disease should become manifest when the normal vital 
energy is reduced or when, as a result of disease, the efforts of 
physiological adjustment must become more strenuous to maintain 
the needful outflow and normal distribution of the blood mass. 
The older writers in this field were prone to attribute the pulsus 
paradoxus to mechanical interference with the normal blood flow, 
basing their position on the frequency with which the phenomenon 
attends pathological adhesions between the mediastinal tissues. 
The facts that have been rehearsed seem to indicate that mechanical 
abnormalities within the chest may only indirectly cause pulse 
failure, by exaggerating certain reflexes which under perfectly 
normal conditions are masked. 

"As already stated, failure of the elevated pulse does not seem 
to occur in persons showing signs of general arteriosclerosis. The 
thought may not be far amiss that this constant organic tendency 
of later life may in itself be a compensation which, by diminishing 
the distensibility of the vessels under the hydrostatic pressure of 
the blood, may more or less substitute that constant and necessary 
redistribution of the blood mass which has become impossible to 
a senile vasomotor apparatus" (L. Hill). 

Goldthwaite 1 classifies the essential hypotensive individual as 

1 Shattuck Lecture, An Anatomical and Mechanistic Conception of Disease, 
Boston Med. and Surg. Jour., 1915, clxxii, 881. 



198 ARTERIAL HYPOTENSION 

the "carnivorous type" of man and suggests that the low blood- 
pressure, weak pulse, subnormal matutinal temperature, etc., are 
due tn mechanical causes. According to this conception the absence 
of retroperitoneal fat exposes the sympathetic ganglia and the large 
bloodvessels which lie unprotected on the anterior surface of the 
spine, to irritation and pressure except when the individual lies on 
his face or his side. This perhaps also applies to the adrenals. A 
long mesentery by dragging downward in the erect posture favors 
splanchnic stasis; ami the low diaphragm with its small respiratory 
excursion due- not efficiently aid the propulsion of blood from the 
abdominal to the thoracic cavity. While these anatomical factors 
perhaps cannot alone account for the symptoms, they are quite 
sufficient to do so when we add the faulty standing and sitting 
postures which are habitually assumed by individuals of this type. 

The most constant finding in the class of individuals under consid- 
eration is arterial hypotension. They often have varying degrees 
of gastroptosis but so do many apparently healthy people whose 
blood-pressure is normal and who have no gastric symptoms so 
long as their nerve tone is up to par. It would seem, therefore, that 
the splanchnoptosis is not the underlying causative factor, although 
it unquestionably acts an important part in some cases. "We 
further ask ourselves whether the hypotension is the cause of the 
nervous manifestations or whether a lack of proper nervous stimuli 
is the cause of the hypotension? This question cannot be posi- 
tively answered. Undoubtedly there is a complex interaction of 
these causes by virtue of which the one may deleteriously affect 
the other, from which we could readily construct a beautiful and 
typical example of the "vicious circle" did it seem worth while to 
do so. 

( hronie low arterial pressure has also been attributed to toxemia, 
and eholin salts have been suggested as the active substance. 1 It 
has been claimed by l'opielski and Modrokowski that chemically 
pure eholin would produce a rise, not a fall of pressure, but Mendel, 
(nderhill and Renshaw 2 have shown that the injection of chemi- 
cally pure eholin did produce a short fall of pressure. 

Histamin may be formed in the intestinal tract by the action of 
the Bacillus aminophylus intestinalis upon the amino-acids. This 
substance is said to lower blood-pressure and has been accredited 
with an etiological role in some cases of arterial hypotension. 

Functional or constitutional physiological vasomotor unfitness, 

Morel, AIIhti : Recherch.es but I'origine clinique de ['hypotension, Livre jubilaire 
,|n I-,. Teissier, Lyon, 1910. 

Action of Salts of Cholin on Arterial Blood-pressure, .lour. Pbar. and Exp. 
Therap., 1912, iii, 649. 



ORTHOSTATIC ALBl \i I \ I i;IA I'.i'.i 

owing mainlj in improper nerve balance, seems t<> be the mosl 
satisfactory explanation For tin' majority of cases of afebrile li; po- 
tension. 

Test for Splanchnic Stasis. The degree of splanchnic venous 
stasis may be estimated, as suggested by Oliver, by placing 
pound bag <»l' shot uniformly across the abdomen in a recumbent 
subject. 

1. In the early morning before food has been taken, no blood- 
pressure changes are observed in normal subjed . 

'2. Thirty minutes after a meal, blood-pressure rises 17 to 20 
nun. Hg. A rise of is nun. is considered normal. 
' 3. After vigorous exercise the shot bag causes no rise of pressure, 
but when the subjed is exhausted from exercise a rise of pressure 
can l»e demonstrated. 

If blood-pressure, especially systolic pressure, is higher in recum- 
bency than in the sitting posture, vasomotor weakness of the 
splanchnies, either with or without loss of abdominal muscular 
tone, may l>e assumed (Sewall). 

ORTHOSTATIC ALBUMINURIA. 

In health the assumption of the erect posture produces an 
increased urinary flow, and a relatively increased sodium chloride 

output. In the subjects of circulatory disease the c litionsare 

reversed. In orthostatic albuminuria there is a qualitative change 
which points to a less efficient renal circulation in the standing 
posture. 1 

Numerous observers have commented upon the frequent asso- 
ciation of orthostatic albuminuria and cardiovascular weakness. 
This form of albuminuria is often associated with arterial hypo- 
tension. The thought naturally suggests itself that the albuminuria 
is brought about by the fact that the splanchnic vasomotor appa- 
ratus only insufficiently compensates the blood-pressure changes 
induced by a change of posture, thus leading to vascular changes in 
the kidney and the albuminuria while the patient is erect. 2 The 
exact nature and mechanism of these vascular changes is still in 
doubt. Renal anemia or venous congestion, either as the result of 
increased intra-abdominal pressure or from kinking of the vessels 
in a more or less movable kidney, have been suggested. 

1 Loeb, H. : Klin. Untersuch. u. d. Einfluss von Kreislaufsaenderungen auf d. 
Urinzusammensetzung, Deutsch. Arch. f. klin. Med., 1905, lxxxiv, 579. 

2 Miintzer, E.: Zur Lehre v. d. vaskularen Hypotonien, Wien. klin. "Wchnschr., 
1910, xxiii, 1341. 



200 ARTERIAL HYPOTENSION 

Neither of these explanations is universally applicable. The 
kidneys arc by no means always movable, and increase of intra- 
abdominal pressure on standing occurs in normal individuals. 
Further, why should the albuminuria only appear on rising in the 
morning and not in the afternoon? According to Forges and 
Pribram, 1 the cause lies in a spastic contraction of the renal arteries. 

This type of albuminuria is sometimes seen in convalescence, 
either from fevers or from trauma, which has necessitated a long 
stay in bed, under which conditions the vasomotor response to 
changes of posture are soon lost, so that the individual on assuming 
the erect posture promptly becomes weak and dizzy. 

Hooker found that with a constant mean pressure the rate of 
blood flow and of urinary secretion bear a direct relation to the 
pulse-pressure, whereas the albumin secreted by the kidney varied 
inversely, experimental evidence which is in accord with the findings 
of Erlanger and Hooker in two cases of orthostatic albuminuria. 2 
Recent researches of Bass and Wessler 3 have, however, contro- 
verted a number of the previously described results. They found 
that blood-pressures in children suffering from orthostatic albumin- 
uria differ but little from normal findings. 

"Functional" albuminuria is not infrequently met with at the 
period of adolescence, often in association with anemia and low 
blood-pressure. Dukes, who has observed many of these cases 
classifies them in three categories. 

1. Cases with cold extremities, clammy hands, low- blood-pressure, 
and deficient vasomotor reactions, as shown by syncopal attacks, 
and by a fall of blood-pressure upon rising from a reclining to an 
erect posture. 

2. Cases with very labile but generally high blood-pressures. 
This is the commonest type. 

3. Cases occurring in spare, neurotic, high-strung and generally 
hyperesthetic individuals. 

It is of course well known that posture may affect albuminuria 
even in organic cases, especially those associated with cardiac 
insufficiency. 

The significance of albuminuria may often be more correctly 
interpreted by means of blood-pressure observations. This symp- 
tom maj incur in perfectly healthy young men after forcible exer- 
cise. In association with slight hematuria it is especially frequent 

1 Zur Kentnise d. orthostatischen Albuminuric, Deutsch. Arch. f. klin. Med., 
L907, .v, 367. 

- Jour. Physiol., November I, 1910. 
Blood-pressure in Children Showing Orthostatic Albuminuria, Arch. Int. Med., 
1913, riii, 39. 



[RTHRITIC AND RHEUMATOID CONDITIONS 201 

after boxing bouts, in which "kidney blows" abet its appearance 
(Stanton). The occurrence of albuminuria after trenuou 
is generally attributed to a secondary splanchnic vasodilatation 
which follows the primary vasoconstriction, and which produce a 
temporary renal congestion. Lee 1 in examining 662 apparently 
healthy students found albuminuria in 5 per cent. In some the con- 
dition was transient, in some orthostatic and in others permanent. 
Eight showed a systolic pressure over 1 Id nun. Ik., yet only one 
case was regarded as nephritic and this ease differed from the 
others in having an increased diastolic pressure 100+). 

Paroxysmal hemoglobinuria and hematuria have also been attrib- 
uted to loss of vasomotor equilibrium. The hitter is generally asso- 
ciated with low blood-pressure. Hemoglobinuria is sometimes 
brought on by walking, especially if this is done in a lordotic pos- 
ture. This type of hemoglobinuria has been explained as resulting 
from vasomotor instability causing an abnormal circulatory state 
in the spleen. 2 

ARTHRITIC AND RHEUMATOID CONDITIONS. 

Excluding lesions of a true gouty nature which are usually 
associated with hypertension, there is a large group of so-called 
"rheumatic" ailments whose pathogenesis is still unknown, which 
often occurs in hypotensive individuals and which tends to disap- 
pear when, as the result of a more efficient circulation, better nutri- 
tion of the muscles, joints and fibrous structures has been obtained. 
To this class belong certain cases of lumbago, sciatica, neuritis, 
stiff neck, and "myalgia." Rheumatoid arthritis and "phospha- 
turia" also generally occur in association with low arterial pressure. 

Low blood-pressure is also met with in cases of status lymphaticus 
in which condition, according to Wiesel 3 and Hedinger, 4 it is asso- 
ciated with hypoplasia of the chromaffin system. 

Treatment of Essential Hypotension. — The curative results of 
therapy in arterial hypotension are never brilliant and often dis- 
appointing, and yet in the majority of cases, especially if the sub- 
ject be not too far advanced in life, much can be accomplished. 
The trouble lies in the fact that we are combating an inbred consti- 
tutional weakness and that an arrest of symptoms often only lasts 
as long as the treatment is continued. 

1 Lee, R. I.: Blood-pressure Determinations, Urinary Findings and Differential 
Blood Counts in a Group of 662 Young Male Adults, Boston Med. and Surg., Jour., 
1915, clsxiii, 541. 

2 Porges and Strisower: Deutsch. Arch. f. klin. Med., January 7, 1915, No. 2. 

3 Zur Path. d. chromafEnen System, Virchows Arch., 1904, vol. clxxvi. 

4 Ueber d. Kombination von Morbus Addisonii mit Status Lymphaticus, Frank- 
furter Ztschr. f. Path., 1907, i, 527. 



202 ARTERIAL HYPOTENSION 

The treatment consists mainly in a proper regulation of the 
patient's daily life, the details of which must be supervised with 
the idea of diminishing the factor- which lead to a lowered nerve 
tunc That mental overwork is often largely contributory in 
increasing hypotensioD is corroborated by Bonser's 1 studio, which 
showed that intellectual fatigue among twelve students observed 
was capable of diminishing vasomotor reactions to emotional stimu- 
lation. A complete rest cure in extreme cases may be advisable 
at the beginning. After this a general routine mode of life as is 
generally advised for neurasthenic patients is in order. A few 
points, however, deserve to he emphasized: (1) Requisite rest and 
sleep (an eight-hour allowance of the latter being a minimum). 
2 Relaxation the avoidance of too prolonged mental or physical 
work. The necessity of a small but regular amount of physical 
exercise, preferably outdoor. (3) The avoidance of excesses — diet- 
ary or sexual. (4) Tobacco— these patients are very sensitive to 
tobacco, an excessive use of which is often directly accountable 
for their symptoms. 

Hydrotherapy. — Aside from the foregoing, hydrotherapy is by 
far the most successful method of treatment. The Nauheim bath, 
the Vichy douche 2 or the needle bath may be recommended, but 
almost equally good results may be obtained with the ordinary 
home shower bath. 

The patient is instructed to take a hot tub bath each morning 
on rising, practising active autofriction with rough linen tape wash 
rags or mittens. When thoroughly warmed he is to turn on the 
cold shower, this to be followed by active friction with a rough 
towel. The length of the stay under the cold spray is to be gradu- 
ally increased and after a short trial will be attended by a good 
vigorous reaction, the skin becoming pink and accompanied by a 
pleasant tingling glow. This treatment must be kept up indefi- 
nitely. Where no shower bath is available, cold water may be 
poured over the head and shoulders from pitchers. 

In patients with enteroptosis and with relaxed abdominal muscles 
systematic exercises, calculated to restore muscular tone, or some 
toil 1 1 of abdominal support, are of distinct utility. Massage is also 
beneficial. 

Goodman 3 lias emphasized the importance of daily morning 
calisthenics, especially those which tend to compress the abdom- 

' Psych. Rev., March, L903. 

'• The Vichy douche consists of b needle douche projected downward on the patient 
throughout the duration of the kith, while general ma sage is administered by an 
,-it tendani . 

Arterial Hypotension Associated with a Definite Symptomatology, 
Am. Jour. Mel. Be, 1914, cxlvii, 503. 



ARTHRITIC AND RHEl WATOID CONDITIONS 203 

inal viscera, increase respiratory excursion and strengthen the 
muscles which maintain a correct standing posture. Such exercises 
must i n>t be carried to the point of breathlessness, much les exhaus- 
tion, Imt should l>f gradually increased in severity and duration as 
the individual is trained up to his task. 

Drugs. Strychnin as an adjuvant to increase nerve tone is the 
must generally useful drug, though it has lirect effect on blood- 
pressure. Digitalis is useless unless there be a definite cardiac 
lesion. 

Although we possess numerous drugs which may be used to lower 

I'l l-pressure, few it' any fulfil the purpose of raising blood-pressure. 

Watson 1 found that atropin, camphor, cotarnin, digitoxin and 
strychnin were valueless for thi^ purpose. Physostigmin, which 
ina\ raise pressure, cannol be used in adequate dosage on account 
of nausea and vomiting. Tyramin (said to be the most importanl 
active constituent of the watery extracts of ergot) gave better 
results.' Musser, Jr., lias reported good results following the 
administration of pituitrin (see p. 352 . 

The Termination of Essential Hypotension. '1 he ultimate outcome 
of cases of essential hypotension has, so far as we are aware, not 
been studied. Individuals belonging to this class are of necessity 
seriously handicapped in their career. They cannot, as a rule, 
lead the strenuous life which seems, in this country at least, to be 
fast becoming the "normal." But whether this enforced modera- 
tion lead> to a longer life, with a diminished tendency toward the 
development of arteriosclerotic changes, is an interesting question. 
If our interpretation of the pathology of this condition is correct 
the splanchnic vessels are habitually relaxed and overloaded with 
blood. Does such a condition predispose to vascular disease of the 
intra-abdominal vessels and organs, or does the passive overloading 
with venous stasis exert a less deleterious effect upon the vascular 
wall than an active distention due to a powerful heart and a high 
vascular tonus? Do these individuals later in life develop arterial 
hypertension as the result of splanchnic arteriosclerosis with its 
attendant dangers and discomfitures, or does Nature mitigate these 
tendencies as a compensation for earlier disabilities? These ques- 
tions must await further studies before an answer can be given. 
The case of the puny dyspeptic " weakling" who weathers the storm 
of an acute infection to which the robust "full-blooded" athlete 
succumbs is well known, as is also the lanky dyspeptic who outlives 
his plethoric friends. "Causa latet, res ipse notissima." 

1 The Value of Drugs as Blood-pressure Elevators, Practitioner, 1915, xciv, No. 4. 



CHAPTER VII. 
BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE. 

Practically all febrile infections are accompanied by a fall of 
blood-pressure, although in some, this feature is specially marked. 
The personal equation of the patient of course greatly influences 
the result. In the so-called sthenic fevers blood-pressure is not 
much affected. In asthenic fevers the fall is very pronounced. 
Many of the ill effects of fever are directly due to low arterial 
pressure and it is now generally admitted that death in many 
infections, is quite as much due to vasomotor as to cardiac failure. 
A few microbic toxins (Staphylococcus, pyocyaneus, mallein) seem 
to have hypertensive qualities (Bosc and Vedel). 

Broadly speaking, the extent of pressure fall tends to vary 
directly with the fever, but there are many exceptions to this rule, 
for the reason that the pressure is influenced more by the toxemia 
than by the pyrexia. In severe infections with a weakening circula- 
tion the systolic pressure falls and pulse-pressure decreases. A well- 
sustained pulse-pressure is to be construed as a favorable sign. 

Degeneration of the adrenal glands in infections, especially 
diphtheria, and the experimental production of similar lesions by 
toxin injections have led some authors to recommend adrenalin 
as a therapeutic medium, both on account of its effect in raising 
blood-pressure, and on account of an hypothetical protective power 
in the defense of the organism. 

In 11 cases of infectious disease, .Marx 1 found no lack of epineph- 
rin in the blood, nor was the blood-pressure especially low. The 
amount of epinephrin recoverable from the suprarenal glands after 
death bears no relation to the character of the fatal disease. The 
height of blood-pressure bears no relation to the epinephrin con- 
tent of the glands. The variable results are perhaps due to the 
gradual death of different sets of the glandular cells. It seems 
likely, therefore, that the beneficial effect of epinephrin in shock 
and allied states is due to its vasoconstrictor action. It is therefore 
merely a symptomatic and not a specific means of therapeusis. 

1 [Jebei den ^drenalingehalt der Nebenniere, Med. Klinik d. Stadt. Krankenanst., 
Mannheim, Dissert. Beidelberg, 1912, vol. auriv. 



BLOOD-PRESSl RE l\ AC\ VE INFECTIOUS DISEASE 205 

Elliot, 1 on the other hand, found that the store of epinephrin in 
the adrenal glands is diminished l»,\ fright, anesthesia, cerebral 
injury and bacterial intoxications. The residual epinephrin has 
been found especially low after death from pneumonia, although 
diminished amounts were also found after measle , scarlatina, acute 
febrile tuberculosis, malignanl endocarditis. Since the adrenal 

glands are not considered res] sible for the normal maintenance 

of blood-pressure, but are regarded as emergency organs, this 
would indicate that in order to combat the hypotension entailed 
by these infectious proeesses the adrenals had heen called upon l'<>r 
a reserve supply, and showed a corresponding exhaustion. The 
decrease of residual epinephrin encountered was never sufficient 
to account for circulatory failure. 

During acute infections a high diastolic pressure has been said 2 
to indicate splanchnic stasis and in seriouslj ill patients to be of 
bad prognostic significance. A low systolic and diastolic pressure 
does not indicate heart failure as much a- it doc-, diminishing vis- 
ceral tone, but a rising diastolic with a falling systolic pressure does 
point toward cardiac weakening. 

During the height of continuous fevers, blood flow at the periphery 
is somewhat slower than in health. The condition- are quite 
different when bodily temperature is artificially raised by the 
external application of heat. In the latter ease, as was shown by 
Hewlett and Van Zwaluwenburg, 3 the peripheral circulation is 
enormously increased, just as it is when a person sweats owing to 
the high temperature of a room. In fevers the vessels still dilate 
under the influence of external heat, but the heightened tempera- 
ture of the body does not influence the heat-regulatory mechanism 
in such a way as to cause their dilatation. The experimental 
researches of Newburgh and Lawrence^ indicate that, in lower 
animals degrees of hyperthermia not greater than those encoun- 
tered in infections are sufficient to cause marked hypotension. The 
increased body temperature of infection is a potent factor in the 
production of the lowered blood-pressure which occurs in such con- 
ditions. The hyperthermia may be the entire cause of such hypo- 
tension. A temporary rise of pressure sometimes accompanies the 
outbreak of the rash in the exanthemata — scarlatina, morbili, 



1 Pathological Changes in the Adrenal Glands, Quart. Jour. Med., 1914, viii, No. 29. 

2 Schwartzmann: Zentralbl. f. inn. Med., August 1, 1914. 

3 The Effect of Room Temperature upon the Blood Flow in the Arm, etc., Heart, 
ii, 230. 

4 The Effect of Heat on Blood-pressure, Arch. Int. Med., 1914, xiii, 287. 



206 BLOOD PRESSURE IN ACUTE INFECTIOUS DISEASE 

variola, etc. 1 The work of the heart is increased during fever if 
the blood-pressure remains constant. 2 

Convalescence from prolonged fevers is attended by a loss of 
splanchnic tone, in pari due to depressed nervous influence and in 
part to weakening of the arterial musculature. When the patient 
assumes the erect posture there is a marked falling of the maximal 
pressure, even when the minimal pressure remains unchanged. 
This diminishes the pulse-pressure, as a result of which the defi- 
ciency of cerebral blood supply must be compensated for by an 
increased pulse rate, which throws an unnecessary strain on the 
heart. Tliis condition is often associated with cardiac murmurs, 
accentuations, reduplications or arrhythmia. Minor degrees of 
physical exertion may cause a fall of 30 to 40 mm. Hg. Under such 
conditions the patient should not be allowed to leave his bed so 
long as there is a marked difference in pulse rate between the erect 
and the recumbent postures. Cardiac erythism and vasomotor 
instability are often encountered. 

As elsewhere actual figures are of little value. It is the course of 
flu' pressure, upward or downward, or marked lability, which is of 
importance. For this reason pressure readings should be made and 
charted simultaneously with the temperature. Marked fluctua- 
tion^ in the height of the systolic pressure are of serious import. 
Many of the older reports on blood-pressure in infectious disease 
are practically useless because they record only the systolic pressures, 
and even these were often made with unreliable instruments. 

The fact is generally recognized that practically any infection 
may produce cardiovascular damage. Thayer found that individuals 
who had passed through attacks of typhoid fever showed a dispro- 
portionately higher pressure in later life than those who have not 
had this disease. 'Die lesson is obvious: that convalescents should 
be spared all unnecessary activity for prolonged periods of time. 
Schwartzmann's 3 recent studies led him to conclude that in infec- 
tious diseases a high diastolic pressure indicates a tendency to 
splanchnic stasis a severe infection. A fall of both systolic and 
diastolic pressure points to vasomotor weakness, whereas a fall of 
the systolic, associated with a rise of the diastolic pressure shows 

cardiac failure. A g 1-sized and well-sustained pulse-pressure is a 

favorable sign. 

l Weigert, K.. Verhalten '1. art. Blutdrucks bei akuten [nfektionskrankheiten, 
Volkmann's Samml. Klin. Vortr., L907, X". 159; Inn. Me.]., exxxviii, 65. 

*Wolf, II. !•'.: The Influence of Temperature on the Output of the Beart, broh. 
[nt. Med., L9J l. viii, 163. 

KUniache Bedeutung der Feststellung d. Bystolischen u. diastolischen Blutdruck 
bei [nfektionskrankheiten, Ztschr. f. inn. Med., L9I4, axv, 745. 



DIPHTHERIA 207 

The venous pressure tends to fall with the arterial pressure in 
infectious disease, but when cardiac failure begins venou 

rises. 

ACUTE INFECTION. 

Cholera. In this disease the specific gravity of the U 1 may 

rise to LOGO to 1 .070, due to loss of fluid, and systolic blood-pressures 
as low as 70 nun. I rg. are no1 rare. 

In the algid stage, according to Lang, ] the pulse-pressure decrea i 
owing to a Fall of the maximum and a rise of the minimum pressures. 
Diastolic pressure diminishes onlj in severe cases. These changes 
arc due to loss of the liquid constituents of the blood and to conse- 
quent vasoconstriction. Saline transfusions averaging 2 liters are 
generally sufficient in restore the total volume of blood and bring 
the pressure relations back to the normal. Larger transfusions 
often lead to supernormal values as the bypertonicity of the vas- 
cular system tends to continue for -nine time and the pulse rate to 
rise. Following the algid stage and during the "typhoid" stage an 
increased blood-pressure is the rule. 

The blood-pressure is therefore a satisfactory criterion of the 
amount of saline infusion to be administered. When given in too 
large quantities an unnecessary amount of work is tin-own upon 
the heart. The judicious employment of saline infusion with epi- 
nephrin has in one epidemic at least greatly lowered the mortality 
of cholera.'- During the recent epidemic in Serbia vaccine was 
administered in large doses of physiological salt solution with defin- 
itely beneficial results. 

Diphtheria.- -Cardiovascular disturbances occur in about in 
per cent, of all diphtheria cases. Death is due to (I I the effect of 
the toxin on the vasomotor centre, heart, and adrenals; (2) to myo- 
cardial lesions (chiefly parenchymatous); (3) to involvement of the 
stimulus conducting system; (4) to bronchopneumonic manifes- 
tations. 3 

Experimental Data. — The experimental injection of diphtheria 
toxin does not always cause an immediate fall of blood-pressure. 
Such a fall occurs some time after the injection of cultures and 

1 Ueber den arteriellen Druck bei Cholera asiatica u. s. Veraenderungen unter d. 
Einfluss grosser Kochsaltzinfusionen, Deutsch. Arch. f. klin. Med., 1912, cviii, 236. 

2 Rogers, L. : A Second Season's Experience of Hypertonic Transfusions in Cholera 
Controlled by Observations on the Blood Changes, Therap. Gazette. November, 
1909, xxiii, 761. 

3 Leede, W. H.: Beitr. z. Diphth. mit besonderer Beracksichtigung d. path, anat., 
Organ u. bacteriologischen Leichenblutbefunde und ihrem Verhalten zum klinischen 
Bilde. (3671 cases). Ztschr. f. klin. Med., 1913, lxxvii, 297. 



208 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

appeals suddenly. 1 Romberg and Paessler showed that in the 
early stages at least the hypotension was vasomotor in origin, but 
vim SlejskaU was able to show a direct toxic action upon the heart. 
Lethal doses of diphtheria toxin after a latent period of twenty-four 
hours produce a marked fall of pressure up to the point at which 
death occurs. The timely injection of antitoxin delays this fall of 
pressure and in sufficient dosage prevents death, but even in exces- 
sive dosage fails to restore a pressure which has already fallen 
dangerously low. 2 MacCallum's 3 experiments indicate that the 
death which occurs at the height of an attack of diphtheria is not 
exclusively the result of direct cardiac injury, although that may 
have a part in the process. Porter and Pratt 4 found that even in 
the late stages of lethal diphtheria intoxication the vasomotor 
centre still responds to both pressor and depressor stimuli, showing 
that death is not primarily due to vasomotor paralysis. Myers 
and Wallace 5 have shown that although the larger bloodvessels in 
intoxicated animals responded normally, the arterioles and capil- 
laries in the splanchnic domain fail to react normally to epinephrin 
and are found in an engorged condition. It appears, therefore, 
that peripheral splanchnic paralysis accounts for the hypotension 
of diphtheria. 

Clinical Data. — Diphtheria is accompanied by low arterial ten- 
sion, the degree of which often stands in proportion to the severity 
of the attack. The highest readings occur in the first and the 
lowest in the second week of the disease, normal tension being 
reestablished by the seventh week. Laryngeal cases, especially 
those requiring operation, show a higher pressure as a result of 
asphyxia. Tracheotomy is often followed by a sudden fall (20 to 
in iniii.!. Pressure in the early stages is ordinarily not much 
affected by serotherapy; in the latter stages it may rise 40 per cent. 
In eases manifesting anaphylactic phenomena there is a great fall 
of pressure (see p. 219). 

Circulatory weakness is a prominent feature of the disease, and 
the normal postural blood-pressure changes are often absent or 

1 Beck and Slapa: Ueber d. Einflusa d. Diphtheriegiftes a. d. Kreislauf, Wien. 
klin. Wrlmsdir., L895, vol. xviii. 

Meyer, I >.: Beitr. z. Kenntnisd. Diphtherievergiftung, etc, Arch. f. exp. Phar., 
1909, X". »in. 

I he Mechanism of Circulatory Failure in Diphtheria, Am. .lour. Mod. Sc, 
MM t. cxlvii, 37. 

•The Slate of the Vasomotor Centre in Diphtheria Intoxication, Am. .lour. 
I'hysiol., xxxiii, 431. 

The Vascular Response in Poisoning from Diphtheria Toxin, Proc. Soc. Exper. 
Biol, and Med., L914, xii, 43. 



ww. w;/ i 209 

reversed even during convalescence. 1 The onsel of nephritis is not 
always accompanied by an increase in blood-pressure. 

There is no fixed relation between fever and blood-pressure. The 

fall of the latter is due to the absorpti >f toxins, as shown by 

animal experiments. The most marked fall in pressure occurs in 
those cases in which antitoxin treatmenl has been delayed. When 
the fall of pressure is marked there is usually more or less cardiac 
involvement, [ntravenous saline injection sometimes produces 
temporary improvement, probably by diluting the toxins. 2 A fall 
of pressure after an amelioration of acute symptoms is often the 
firsl sign of persistent toxemia." 

Fatal cases sometimes show a marked fall of pressure several 
days before the lethal termination. A progressive fall of tension is 
of had prognostic import, as is also a unilateral pressure difference, 
but high pressure does not of necessity presage a recovery. 

As a means of differential diagnosis between true diphtheria and 
simulating infections, blood-pressure readings are valueless. The 
occurrence of paralysis is sometimes preceded by ;i fall of pressure 
(Kolossova) . 

Malaria. — -According to Federn, blood-pressure rises during the 
chill and falls during the period of sudation. In chronic malarial 
cachexia, hypotension is the rule. Lemirne 4 has reported verj low 
blood-pressure in pernicious malaria associated with cramps, weak- 
ness, lumbar pains, and white dermatographism, the autopsies 
revealing hemorrhagic and necrotic suprarenalitis. 

If some of the recent hypotheses regarding malaria, which are 
based upon facts discovered since the artificial cultivation of the 
Plasmodium has become possible, should prove true, blood-pressure 
may have a more important bearing upon malaria than has been 
supposed. It has been suggested that after attaining a certain 
size the plasmodium reaches and lodges in the capillaries and that 
in this situation the inoculation of new 7 corpuscles normally takes 
place. The debris and pigment which result from their destruction 
may, if the infection be severe, "plug" the brain capillaries and 
produce "cerebral malaria." Further, the height of the blood- 
pressure and the state of capillary dilatation or constriction would 
influence the stage at which the organisms would recede from the 

1 Rolleston, J. D.: Blood-pressure in Diphtheria, British Jour. Children's Dis., 
October, 1911, viii, 28. 

2 Cobliner, W.: Blutdruckmessungen bei erwachsenen Diphtheriekranken, Dissert., 
Berlin, 1912, p. 45. 

3 Schoen, C: Deutsch. med. Wchnschr., March 27, 1913. 

4 Bull, de l'Acad. de med., October 17, 1916. 

14 



210 BLOOD-PRESSURE IX ACUTE INFECTIOUS DISEASE 

peripheral blood stream into the capillaries to undergo segmenta- 
tion, or destruction, or to invade new blood cells. At this point, 
too, the organisms would be immune to the effects of quinine which, 
according to this view, is not directly toxic but merely increases the 
permeability of the red cell to the normal destructive serum. 1 

Meningitis. Epidemic Cerebrospinal Meningitis is almost con- 
stantly associated with high intracranial tension. Moderately 
increased blood-pressure is not infrequently seen in the early acute 
stage, during exacerbations of symptoms late in the disease, or 
where the malady assumes a chronic aspect. Often the higher the 
pressure the more severe the case. The withdrawal of cerebro- 
spinal fluid by lumbar puncture, while usually attended with a fall, 
has no constant effect on blood-pressure. It seems, therefore, that 
increased intracranial tension in meningitis does not necessarily 
cause a rise of blood-pressure unless it be late in the disease, when 
internal hydrocephalus may develop as a result of blocking the 
foramina of the fourth ventricle. 2 

Tuberculous Meningitis. — In tuberculous meningitis arterial press- 
ure is but slightly elevated, the readings obtained are about nor- 
mal; whereas in tuberculous disease they are generally subnormal. 
In other forms of meningitis very high pressures are sometimes 
encountered (230 mm.) which sometimes tend to run a parallel 
course with the increased pressure of the cerebrospinal fluid. 3 

Since meningitis is sometimes treated by intraspinal injections 
it is important to know how high the intraspinal pressure may be 
raised without danger. It has been found experimentally that 
although there is a marked difference in sensitiveness in different 
individuals, a sudden increase of pressure is always more dangerous 
than a gradual one. The first mechanical effect is upon the respira- 
tory centre, followed quickly by profound cardiac inhibition which 
causes a sudden and tremendous fall of blood-pressure. Inasmuch 
as this is not a vasomotor disturbance, epinephrin is not indicated. 
In fact, it would probably do harm on account of its cardiac inhibi- 
tive effect.' The best results are obtained through the use of 
cocain and atropin, the former stimulating the respiratory centre 
and the latter lessening cardiac inhibition. (See Lumbar Puncture.) 



1 Jour. Am. Med. Assn., 1914, lxii, 1330. 

- Robinson, G. C: Blood-pressure in < lerebrospinal Meningitis, Arch. Int., Med. 
M ■ ■ L910, p. )v-'. 

Parisot, J.: La pression arterielle dans les meningites, Soe. Med. do Nancy, 
December 8, L909; Rev. Med. de I'Est, 1910, p. 48. 

•Carter, W. B.: The Effect of Intraspinal Injections of Ringer's Solution in 
Different Amounts under Varying Pressures, Arch. Int. Med., 1912, x, 425. 



PNEUMOM 1 21] 

Pneumonia. —The view thai death from pneumonia frequently 
results from peripheral vasomotor paralysis has been quite generallj 
held, despite the facl thai clinical observations are not at all unani- 
mous in supporting this view. Among L9 fatal cases, and 26 ca e 
which recovered, Newburgh and Minol found thai the systolic 
pressure in the fatal cases was continuously above that in the cases 
which recovered. 

In 1899 Romberg and his associates endeavored to tesl the state 
of the vasomotor mechanism by the use of stimuli to the skin and 
mucous membranes. After producing a fatal pneui ioccus septi- 
cemia in rabbits, blood-pressure was observed in the animals after 
electrical stimulation applied to the nasal and anal mucous mem- 
brances. In the early stages of the disease sensory stimuli always 
caused a marked elevation of blood-pressure. At a later period, 
when the appearance of the animals suggested the approach of 
death and the temperature was falling, the reflexes were -till present 
but did not attain the normal height. Finally, when the animal 
was in a state of collapse and death was imminent no rise of blood- 
pressure followed, peripheral stimulation. As a result of their 
observations, Romberg and his co-workers believed thai they had 
proved that death in acute infectious diseases was the direct out- 
come of paralysis of the vasomotor centre in the medulla. 

This, it is to be observed, is an experiment of a negative sort, 
since it rests entirely upon failure to obtain certain physiological 
responses . 

Porter and Newburgh 1 have- recently completed experiments 
from which they obtained positive information regarding this 
problem. 

They produced not only pneumococcic septicemia in rabbits, 
but also acute fatal pneumonia in rabbits, cats and dogs. In order 
to judge of the condition of the vasomotor apparatus, they measured 
the vasomotor reflex. But instead of using precarious reflexes from 
the mucous membranes, Porter and Newburgh exposed and cut 
the depressor and the sciatic nerves and stimulated the central ends. 

The data obtained are probably more reliable than those first 
mentioned, since the depressor nerve is composed entirely of fibers 
which affect the vasomotor centres, whereas other nerves contain 
fibers of widely different function. As a result of these experiments 
they found that the vasomotor centre was not impaired in any of 
the examples of fatal pneumonia studied. 

1 The State of the Vasomotor Apparatus in Pneumonia, Am. Jour Physiol., 1914, 
xxxv, 1. 



212 BLOOD PRESSURE IX ACUTE IXFECTIOUS DISEASE 

It is not surprising, therefore, that low blood-pressure in pneu- 
monia is not invariably of evil omen, indeed the systolic pressure 
i- often higher in fatal than in non-fatal eases, and hence Gibson's 
rule is far from infallible. The rate of the pulse and not the blood- 
pressure level, is the chief factor in deciding whether the pressure 
will or will not fall below the pulse. 1 

On the other hand, as opposing the view that pneumonic death 
is primarily a cardiac failure, it has been shown that: (1) The heart 
muscle is not functionally impaired in pneumonia since the pneu- 
monic ventricle heats normally as soon as its food is normal; (2) 
pneumonic blood, suddenly fed to a normal heart muscle, lowers its 
efficiency, lessening the duration and the area of contraction; (3) 
the heart muscle in pneumonia gradually exposed to the action of 
tin poison, largely adjusts itself to its poisoned food. 2 Insofar as 
experimental data go, therefore, we are left in a quandary. The 
vasomotor centre is not impaired and the heart muscle is still effi- 
cient, yet the patient dies a circulatory death. In answer to this 
Porter has suggested that the brain centre which controls arterial 
tonus, and that which regulates vasomotor reflexes, are not identical. 
Another explanation offered by Boothby 3 is that there exists a 
subordinate circulatory centre which acts in combination with the 
respiratory centre. 

1 >eath in pneumonia is often attended with the same symptoms 
as those produced by surgical "shock." There is often no dilata- 
tion or engorgement of the right heart. In lobar pneumonia there 
is, in addition to hypotension, the added mechanical obstruction 
in the lungs with which the right heart has to cope. Pulmonary 
involvement is often extensive, but experiments have demonstrated 
thai one-sixth of the total lung capacity is sufficient to maintain 
life, 4 and in the advanced stages of tuberculosis an individual often 
lives for weeks or months with very little lung tissue intact. It is 
not, therefore, the extent of the pulmonary lesion which is of pri- 
mary importance in pneumonia but the degree of toxemia, and this 
is often reflected in blood-pressure estimations. 

The Pulse Rate Blood -pressure Ratio. — Gibson suggested that the 
ratio of pulse rate and blood-pressure may be of some prognostic 



1 Newburgh and Minol : Arch. Int. Med., I'.M 1, tiv, Is. Newburgh: Am. Jour. 
Med. Be, February, 1915, i>. 204. 

- Newburgh, I>. II., and Porter, M. T.: The Hearl Muscle in Pneumonia, .Tour. 
Exper. Med., 1915, xxii, L23. 

J. .in. \m. Med. \--n.. L915, Lxv, 959, 

Hi, I-.. I.i' Play, Mantoux, ('.: Capacite pulmonaire minima compatible 
avec la vie, Jour, de phyaiol. Exper., 1913, xv, 16. 



PNEl MONIA 213 

value. "A pressure appreciably below the norma] in pneumonia 
is invariably of evil omen, and any considerable fall bodes di 
When the arterial pressure, expressed in millimeters of mercury, 

docs not fall below the pulse rate expressed in beats per minute, 
the fact may be taken as of excellent augury, while the '-on 
equally true." This statement has found corroboration from some 
sources but is certainly far from infallible. ' 

The pulse-pressure ratio must not lie accepted too literally ; for 
individuals who have habitually a high pressure may, when criti- 
cally ill, show a more favorable ratio than their condition justifies. 
On the other hand, patients with essentia] hypotension may show 
a lower pressure while their actual condition may he quite satis- 
factory. Howell- has found thai in doubtful cases observation of 
the relative intensity and duration of the lir-i lour auscultatory 
phases may he distinctly helpful. Strong, clear-cut sounds over an 
artery are indications of circulatory strength. This applies especially 
to the third phase in pneumonia. 

"More is to he gained from watching the changes in a succes- 
sion of sequences than from isolated observations, for, indeed, one 
patient may be quite comfortable with a sequence which in another 
promises the worst." In pneumonia the persistence of the second 
phase, which is most readily lost, is of favorable import. All clear 
tapping sounds are of good augury, whether heard in thai part of 
the sequence usually assigned to the third phase or not, whereas 
feeble, muffled sounds must be considered as unfavorable. " When 
the clear tap is lost and the sequence appears as a succession of 
dull, muffled sounds from systole downward, a high grade of per- 
ipheral relaxation and secondary cardiac exhaustion can be inferred. 
When to this arrhythmia is added, the worst picture is drawn." 

There is no constant relation between blood-pressure and the 
occurrence of crisis. As a rule pressure is lower after the crisis 
than before, and a gradual return to the normal occurs pari passu 
with convalescence. Hypertensive cases often have a lowered 
pressure during the course of the disease. 

Venous pressure is low, but rises as cardiac weakness increases. 

The beneficial effects of cold fresh air are unquestionable, but 
they cannot be explained as the result of any direct effect upon 
blood-pressure. A slight rise of systolic pressure of variable dura- 



1 Goodman and Pitman: Therap. Gazette, July 15, 1911. Tice: Am. Jour. Med. Sc, 
1916, clii, No. 1. 

2 Possibilities in the Use of the Auscultatory Method of Determining Blood- 
pressure in Pneumonia, Jour. Am. Med. Assn., 1914, lxii, 1230. 



214 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

tion is produced in normal adults by exposure of the face to cold 
air, but is often followed by a fall to the original level even while 
the exposure is continued. 1 Van Ordt, s it is true, found a slight 
rise of blood-pressure following exposure to cold, but not greater in 
amount than the normal physiological range. Barringer obtained 
practically negative results, regardless of whether the entire body 
or only the face was exposed. 

In children, however, I lowland and Hoobler 3 always found a rise 
of pressure beginning one hour after exposure to cold air, reaching 
it^ maximum in two hours, and persisting as long as the child was 
kept out. Return to the ward was followed in twenty minutes 
by a fall which reached its maximum in one hour. Reexposure 
induced a second rise. Convalescents showed less striking results 
than the febrile eases. In warm weather the pressor effect of out- 
door air was lacking, showing that the vascular reflex was due to 
the low cicd temperature. Only the face being exposed, the increased 
blood-pressure probably resulted from central vasomotor constric- 
tion, resulting from stimulation of the nasal mucosa. These find- 
ings are directly at variance with those of Morse and Hassman. 4 

Sonic cases of type I pneumonia show an increased pressure 
( 10 to 15 mm.) both systolic and diastolic after the administration 
of serum. 

Scarlet Fever. — The fall of pressure, w r hich occurs in about 25 
per cent, of the cases, 5 is less than in typhoid fever, and stands in 
direct relation to the severity of the attack. It appears during the 
period of eruption and is pronounced during febrile defervescence. 
In mild cases pressure is but slightly affected. In grave cases a 
marked fall is associated with a high temperature and a rapid pulse. 
The normal is gradually reestablished during convalescence, more 
slowly after severe cases. Slight albuminuria may not be accom- 
panied by a rise of pressure. 6 In scarlatinal nephritis, blood-pressure 
sometimes rises before albumin has appeared in the urine. Cardiac 
involvement is sometimes associated with a slight rise and marked 
lability of arterial pressure (Weigert). Dietary modifications — 



1 Barringer, 'I'. B.: The Effect <>f Cold Air upon the Circulation in Healthy ami 
Sick Individuals, Am. Jour. Mel. s.-., L912, cxliv, '-'•';::. 
■ r. f. Diat. u. physik. Therap., 1905, ix, :t:ts. 
Effect "f Cold, I resb \ir on the Blood-pressure in Pneumonia in Children, Am. 
Jour. Di-. Child., 1912, iii. 294. 

•Am. Jour. Dis. Child., November, 1916. 

'• Rolleston, .1. I).: The Blood-pressure in Scarlet Fever, British .lour. Child. Dis., 
1912, i\. 111. 

I . i rier and Tanon: Le Pression arterielle dans la Scarlatine de FAdulte, Jour. 
Physiol. <-i Path. Generate, 1908, x, 481. 



TYPHOID AND PARATYPHOID FEVER 215 

milk, salt, salt-free food — and minor complications have bu1 little 
effect on Mood-pressure. 1 

Smallpox. — The pustulation stage is associated with a fall of 
arterial pressure which compares in degree to the toxemia. A 
return to the normal during convalescence occurs very slowly. 2 

Typhoid and Paratyphoid Fever. — The blood-pressure in typhoid 
fever falls below the normal after the patieul takes to his bed and 
remains low until convalescence is established. This is the result of 
toxic vasomotor depression. The fall of pressure hears no constant 
relation to the pulse or temperature curve or the severity of the 
attack, but a rapid or progressive fall of pressure is often of serious 
augury. The value of blood-pressure readings as a means of differ- 
ential diagnosis or prognosis is not of much value. 3 

Both systolic and diastolic pressure fall during the later febrile 
period, and rise coincidently at the beginning of the afebrile period. 
Later on in convalescence the systolic and diastolic levels move 
farther and farther apart, owing either to a systolic pise and a 
diastolic fall or because the one pressure remains stationary while 
the other recedes from it. Finally, sometimes suddenly and at 
times coincidently with leaving bed, both pressures attain a higher 
level. Studies of the "pulse-pressure quotient - ' and the "amplitude 
frequency product" indicate that during the febrile period the 
heart performs increased work despite the lowered pressure, and 
that circulatory weakness is in part cardiac and in part vasomotor 
in origin. Further, that in one case which came to autopsy, toxemia 
was accountable for the condition, since no microscopic myocardial 
lesions were encountered (Fig. 87).- 1 

In 115 cases the average pressure was found to be: First week, 
115 mm.; second, 106 mm.; third, 102 mm.; fourth, 96 mm.; fifth, 
98 mm. The occurrence of perforatum is often followed within two 
to four hours by a rise of from 20 to 70 mm. It is caused by (a) 
pain, and (b) beginning peritonitis, in the early stages of which 
condition a marked pressure increase is often seen. 5 In the later 
stages a toxic paralysis of the vasomotor and respiratory centres 
in the medulla occurs (Romberg and Heineke). 

1 Nobecourt and Teissier: La Pression arterielle dans la Scarlatine de l'Adulte. 
Jour. Physiol, et Path. Generate, 1908, x, 481. 

2 Davidson: Blood-pressure in Fevers, Lancet, October 19, 1907. 

3 Weigert, K. : Ueber d. Verhalten d. arteriellen Blutdrucks bei d. akuten Infek- 
tionskrankheiten, Samml. klin. Vortrage, 1907, xvi, No. 9. 

4 Dietschy, R., and Hossli, H. : Beitriige z. Beurteilung d. Kreislaufsverhaeltnisse 
bei Infektionskrankheiten, etc., Deutsch. med. Wchnschr., April 24, 1908, vol. xciii. 

6 Crile, G. W. : The Diagnostic Value of Blood-pressure Observations in the Diag- 
nosis of Typhoid Perforation, Jour. Am. Med. Assn., 1903, xl, 1292. 



216 BLOOD-PRESSURE IN ACUTE 1XFECTI0US DISEASE 

The occurrence of a relapse bears no constant relation to blood- 
pressure. In some cases this phenomenon is preceded by a rise, in 
others by a fall of pressure. 



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I h.. 87. Record of a rapidly fatal case of typhoid 
fever in which death apparently resulted from cardiac 
weakness. The systolic pressure falls, the diastolic 
re rises, the quotient and the amplitude fre- 
quency product steadily decline, while the venous 
pressure and the pulse rate rise. Microscopic exam- 
ination of the bear! being negative, death was 
l to toxic factors. (Dietschj and Hdssli.) 



Fig. 88.— Key to Fig. 
87: a, maximum pressure; 
6, minimum pressure; c, 
temperature; d, pulse rate; 
e, blood-pressure quoti- 
eni ; ./', pressure of the 
jugular vein. 



During convalescence there is a slow, gradual rise of pressure 
(sometimes interrupted by temporary drops), which increases more 



TYPHOID I \i> r \.R \ I ) PHOID / /. I ER _h 

rapidly when the patient is again up and about. Rolleston 1 found 
that 93 per cent, of his cases showed a fall of pressure oil assuming 
the erect posture. This observation, represents the usual occur- 
rence of cardiac and vasomotor weakness which an attack of typhoid 
fever entails. I have found the employmenl of Crampton 
useful guide regarding the length of time which convalescents may 
be permitted to sit up or the amount of exercise in w hich they may 
be allowed to indulge. Not infrequently blood-pressure remains 
subnormal for weeks and even months after the actual fever has 
subsided. 

Thayer 2 pointed out the fact that patients who had had typhoid 
fever not infrequently showed evidences of arteriosclerosis and 
arterial hypertension out of proportion to their age. Hemorrhage 

is usually followed by a fall, sometimes ;i marked fall, of pt 

(20 to 40 mm.). In cardiac weakness marked diurnal variations 

may occur. 

Cold sponging raises the pressure 10 to L5 mm. in cases which 
respond favorably to the treatment; in the cases which become 
cyanotic, this rise does not occur. A complicating pneumonia 
may temporarily raise the pressure, as may also the psychic effeel 
of too many visitors. 3 To be of any value in typhoid fever blood- 
pressure observations should be made twice daily. The normal 
individual range will then be established and changes definitely 
demonstrated. If perforation is anticipated readings should be 
made at half-hourly intervals. 

Loeper 4 has reported low blood-pressure associated with cyanosis, 
myalgia and diarrhea occurring on the evening or the day following 
the first dose of antityphoid inoculation. These symptoms were 
relieved by epinephrin, which he believes should be used as a pro- 
phylactic. 

The Treatment of Febrile Hypotension. — Hypotension per se is not 
a symptom calling for treatment any more than is hypertension. 
The resting body can do with a pressure well below the normal 
without deleterious effects; indeed, this may be a method of con- 
serving energy. Only when pressure falls progressively or is accom- 
panied by other signs of cardiac or vasomotor failure is interference 
warranted. Many a case of typhoid fever or pneumonia weathers 
the attack satisfactorily, having a systolic pressure of about 100 
mm. Hg., without stimulation. 

1 Blood-pressure in Typhoid Fever, Med. Press and Circular, March 15, 1916. 

2 Bull. Johns Hopkins Hosp., 1904, xv, 313; Am. Jour. Med. Sc, 1904, exxvii, 391. 

3 Barach: Blood-pressure in Typhoid Fever, N. Y. Med. Jour., August 24, 1907. 

4 Presse Medicale, October 19, 1916. 



218 BLOOD-PRESSURE IN ACUTE INFECTIOUS DISEASE 

When, however, a falling pressure is associated with an increased 
pulse rate, pallor, sweating, cold extremities, and other signs of 
collapse, direct treatment, calculated to restore vasomotor tone, is 
indicated. It is generally easier to keep up pressure by early treat- 
ment sponging, etc. — than to restore it once it has fallen to the 
danger limit. The best results will usually be obtained by fresh 
air, cold sponging, saline enteroclysis, or intravenous infusion. The 
addition of from 0.5 to 1 per cent, of sodium bicarbonate to the 
0.8 per cent, sodium chloride solution is advisable. The addition 
of the former salt produces a greater rise of the diastolic pressure 
and seems to exert a definitely stimulating effect upon the heart 1 
(see p. 401). In the course of fever the peripheral circulation, as 
indicated by the flow of blood in the foot, is distinctly subnormal. 
This apparently results from vasoconstriction, an effort on the 
pari of Nature to secure an increased blood flow for the organs 
chiefly involved. According to this hypothesis, fever is due to 
more rapid flow, and therefore increased metabolism of the internal 
organs. Hence, cold sponging would seem to be the most valuable 
form of treatment, since it tends to abet the natural process; whereas 
antipyretic and other vasodilator drugs are directly contra-indicated, 
since they tend to interfere with the natural mechanism of healing. 2 
The application of an ice-bag to the precorclhim is often useful since 
it not only slows the heart but increases blood-pressure. Since 
febrile hypotension is essentially toxic in nature, all available means 
must be employed to counteract or minimize toxemia. Febrile 
hypotension is often associated with tympanites, which symptom 
should be zealously guarded against, since it indicates indigestion 
and malnutrition, and because it seriously embarrasses both 
respiration and heart action. 

Treatment therefore should consist of: 1. Combating Toxemia. 
This is to be accomplished by increasing elimination by attention 
to the emunctories. Proper evacuation of the bowels and increas- 
ing the urinary output are useful measures. The latter is often 
besl accomplished by increasing the fluid intake; by mouth, by 
means of continuous enteroclysis (drip method), by intravenous 
saline infusion or hypodermoelysis. Fresh air plays an important 
role. 

2. I 'o8omotor stimulation, by cold sponging or tubbing, or by the 

1 Dawson: The Changes in the Heart-rate and Blood-pressure Resulting from 
Severe Hemorrhages and Subsequenl Infusion <>f Sodium Bicarbonate, Jour. Exp. 
Mi d . 1905, vii, 1. 

'Stewart, '"■. N.: Blood Flow in the Feet, with Special Reference to Fever, .lour. 
Exp. Med., 1913, xviii, 354. 



MEDICAL OR TOXIC SHOi /. 219 

use of drugs which ad upon the central or peripheral vasomotor 
system. 

The drugs most commonly employed are strychnin, atropin, 
caffein, camphor, digitalis, strophanthus, pituitrin, epinephrin. 
Although they may do good, improvement cannot, excepl in case 
of the last two, be attributed to direct blood-pressure raising 
qualities (see under Therapeutic 

Medical or Toxic Shock. A condition of shock clinically identical 
with that seen after surgical trauma may occur as the result of 
anaphylaxis. The injection of foreign proteins, horse serum for 
instance, is sometimes followed by sudden collapse or even death 
from this cause. A distinction is often made between shock and 
collapse. Iu the former we are dealing with a lowering of vaso- 
motor tone due to insufficient reflex splanchnic stimulation; iu the 
latter the vasomotor paresis is due to depression resulting from 
toxemia. Pearce has shown experimentally that in both anaphy- 
lactic shock and in peptone intoxication in dogs there is a great 
fall of blood-pressure (20 to 30 mm. Hg.) due to splanchnic dilata- 
tion and resulting in medullary anemia. Cardiac and respiratory 
abnormalities are entirely secondary manifestations. 

That there is, however, a difference between toxic -hock and that 
due to hemorrhage, is shown by the different response to nicotin 
and epinephrin. In anaphylactic and peptone shock during the 
hypotensive period the pressor effect of nicotin ma;, be increased 
at a time when epinephrin is ineffective, whereas iu Hie hypoten- 
sion of hemorrhage although the nicotin reaction may be abnormally 
intense, epinephrin still produces vasoconstriction and increase of 
blood-pressure. 1 Simonds believes that this indicates a state of 
reduced irritability in the vasomotor centre, and attributes the 
increased nicotin reaction to its mechanical effect upon respiration. 
The dyspnea so produced causes suction on the overfilled non- 
collapsible veins of the liver and brings sufficient blood to the 
unfilled right side of the heart and ultimately to the systemic ves- 
sels, in which pressure is raised. 

Physiological studies having for their object the determination of 
the mechanism by which the low pressure is caused, demonstrate 
that the condition is essentially a peripheral vasomotor paralysis. 
Pharmacological studies indicate that the effect is on the nerve 
endings rather than on the muscle. 

With independent cerebral transfusion the recovery from low 

1 Simonds, J. P.: Low Blood-pressure not Associated with Trauma or Hemorrhage, 
Arch. Int. Med., 1916, xviii, 848. 



220 BLOOD-PRESSURE IX ACUTE IXFECTIOUS DISEASE 

pressure is more rapid than in the intact animal. This is true also 
when an animal is transfused by carotid anastomosis, and recovery- 
is especially satisfactory when the transfusion is accompanied by 
simultaneous bleeding from the femoral vein. 

The researches of Auer and Robinson 1 indicate that in animals 
at least, the fall of pressure seen in anaphylactic shock may be 
partially cardiac in origin. The electrocardiogram shows variable 
abnormalities, ranging from an increased depression of the S-wuve 
to complete dissociation of stimulus conduction. 

Henderson and Barringer state that "in both hemorrhage and 
circulatory shock the decrease in the venous supply to the right 
heart is the critical factor. In this they differ from vasomotor 
failure, in which the peripheral resistance of the arterial system is 
decreased." 

"The indications for treatment therefore appear to be (1) relief 
of splanchnic congestion, and (2) increase of volume of blood to 
the heart and medulla. Cardiac stimulants alone, or salt solution 
and adrenalin alone, cannot bring about a permanent improvement. 
A combination, however, of the slow injection of adrenalin in salt 
solution (1 to 40,000) intravenously with the addition of a pure 
cardiac stimulant, as digitoxin, leads to relatively rapid and per- 
manent improvement, by promoting a determination of the blood 
to the right heart and increasing the circulation in the brain" 
I Pearce). 2 

As a prophylactic measure in anaphylactic shock, the utility of 
atropin has been demonstrated by Auer. 3 In guinea-pigs without 
atropin, 75 per cent, died; with this drug only 28 per cent, (see 

Surgical Shock, p. 396). 

THE EFFECT OF DRUGS ON THE VASOMOTOR SYSTEM. 

Strychnin, while it may be useful in other ways, does not stimulate 
the vasomotor centre except in toxic doses. 

Epinephrin has no direct effect on the centre, but may be useful 
in emergency for its sympathetic stimulation. 

Camphor is probably without effect on the centre, as is also 
spiirti in. Ergot increases pressure by its stimulation of the sympa- 
thetic nerve. 

I lectrocardiographic Study of the Anaphylactic Rabbit, Jour. Exp. Mod., 
1913, xviii, IV). 

•A Study "I Experimental Conditions "f Low Blood-pressure of Non-traumatic 
Origin, \rchiv. Int. Med., August, 1910, \i, 218; also, A Study of tin- Action of 
the Heart in Anaphylactic Shock in a Dog, .lour. Phari ami Exp. Therap., L912, iv, 
No. 1. 'Am, Jour. Physiol., September, 1910. 



THE EFFECT OF DRUGS <>\ THE VASOMOTOR SYSTEM 22] 

The vasomotor centre is depressed by chloroform; ether stimu- 
lates moderately, if it has any effect. Pituitrin lias bu1 a slight 
action on the centre. It is a useful emergency measure which rai es 
pressure by its action on the peripheral arterial muscle. 1 Alcohol 
is deleterious if increase of pressure i the desideratum. 

If the hypotension results from cardiac weakness, digitalis or 
strophanthin may be tried, although their effects arc often disap- 
pointing in febrile toxemia. An ice-bag applied to the precordium 
is often the most satisfactory method of steadj ing the heart. 

1 Pilchcr and Snllniaiin: Studies od the Vasomotor Centre, Jour. Phar. ai 
Therap., L915, vi, 323. 



CHAPTER VIII. 
BLOOD-PRESSURE IN CHRONIC INFECTIOUS DISEASE. 

Syphilis. Owing to the great frequency of aortitis as a lesion 
of secondary syphilis, and since it so often involves the mouths of 
the coronary arteries, it is not surprising that blood-pressure varia- 
tions and other cardiac symptoms should frequently be encoun- 
tered. Two-thirds of the 22S cases studied by Grassmann 1 showed 
cardiac disturbances— arrhythmia, bradycardia, tachycardia, mur- 
murs, dilatation, etc. He found that the blood-pressure, which is 
normal at first, soon gives place to hypotension and instability. 
As soon as aortic valvular leakage is established, the pressure 
changes take on the characteristic manifestations of this lesion 
(see p. 242). In 80 per cent, of Grassmann's cases the pressure 
(von Basch sphygmomanometer) was below 80 mm. in the tem- 
poral artery. Some of these cases showed a further reduction of 
both pressure and hemoglobin on the institution of the mercurial 
treatment. 

Based upon a study of 50 hypertensive cases, 90 per cent, of which 
yielded either a positive Wassermann or luetin test, Stoll 2 has 
advanced the hypothesis that hereditary syphilis is one of the most 
common causes of hypertensive disease. He lays stress on the 
importance of performing a luetin test, especially if activated 
by a week's mixed treatment in hypertensive cases which have 
yielded a negative YYassennann test. He reports favorable results 
from specific treatment especially in patients with pressures below 
200 mm. Ilg. without any apparent deleterious effects upon the kid- 
ney, even in cases in which the phthalein excretion was consider- 
ably reduced. The best results were obtained by administering mer- 
cury by inunction, and potassium iodide by mouth (see Salvarsan, 
p. 354). Although the actual degree of hypertension is as a rule 
unaffected by antiluetic treatment, occasionally marked reductions 
in blood-pressure are produced. 3 

1 Klin. [Jntersueh. a. .1. KreislauforganeD in Friihstadium d. Syphilis, Deutsoh 
Arch. f. Win. Med., 1901, Ixix, 281. 

•The Role "f Syphilis in Eypertensive Cardiovascular Disease. Am. .lour. Med. 
115, .1. 178. 

• Levinson, L. A.: Results of Treatment in Arterial Hypertension Due to or 
Associated with Syphilid Jour. Am. Med. Assn., 1916, lxvii, 730. 



TUBERCULOSIS 



223 



Tuberculosis. Tuberculous disease is usually mentioned as one 
of the conditions in which arterial tension is subnormal. This 
statement appears to be correct insofar as the late tages of the 
disease are concerned, when toxemia and emaciation arc pronounced. 
In the early stage, especially at the time when the diagnosis is still 
in doubt, normal pressure is found. Janeway's 1 recently published 
charts which are here reproduced, show a close similarity b< I 
tuberculous office patients and normal individuals. These state- 
ments are also corroborated by Shalet, 2 who studied LO00 ca 
the Otisville Sanatorium. 



SYS. 
PRESS. 

140 
135 
130 
125 




































"^ ^^^ 












































































































yj 












































































































^s* / 






-< 


*- 




~x 
























120 


















— « 










NORMAL TUBERCULOSIS 



Fig. 89. — Median systolic blood-pressures, arranged by age periods. Persona] 
observations. (Figures in brackets at right of curves indicate total number of 
individuals observed in each group.) 



DIAST. 
PRESS. 

90 
85 

80 








































... 






















































































III 1 1 










































































































































































































































^"^ 































































































































































































































































































































































































































































Fig. 90. — Median diastolic blood-pressure?, arranged by age periods. Personal 
observations. (Figures in brackets at right of curves indicate total numberjof 
individuals observed in each group.) 

As in health, the pressures are lower in tuberculous women than 
in men. Blood-pressure bears no definite relation to the stage of 
the disease, although it generally does to the degree of toxemia. 



1 Important Contributions to Clinical Medicine during the Past Thirty Years 
from the Study of Human Blood-pressure, Tr. Assn. Am. Phys., 1915, xxx, 27. 

2 Blood-pressure in Pulmonary Tuberculosis, New York State Jour. Med., 1914, 
xiv, 189. 



224 BLOOD PRESSURE IN CHRONIC INFECTIOUS DISEASE 

Thus the pulse rate and the degree of temperature sometimes, 
although by do means always, hear an inverse relation to blood- 
pressure. A complicating nephritis may cause a rise of pressure, 
1 nit rarely, if ever, to the degree attained in non-tuberculous cases. 
In the literature on the subject there is, however, much room for 
uncertainty, since the term "nephritis" as used in connection with 
tuberculosis may mean a tuberculous lesion engrafted on an old 
nephritis, amyloid disease, or a true tuberculous nephritis. In the 
latter condition. Reiner' found actual hypotonia as contrasted 
with other forms of pyelitis and pyelonephritis in which the pressure 
was at least normal if not distinctly increased. 

The vasomotor instability of tuberculosis is shown by the fact 
that at least a large proportion of the advanced cases show a fall 
of pressure and a considerable increase in pulse rate, on changing 
from the recumbent to the erect position. 

Bouchard, Arloing, Rhodet, and Tom-mount believe that the 
toxin of the tubercle bacillus possesses distinct vasomotor influ- 
ences. These results have been corroborated and much more satis- 
factorily demonstrated by Emerson. Man is apparently much 
less sensitive to this effect than animals, since a relatively larger 
and more concentrated dose is required to produce much fall of 
pressure. ^Whether this toxin is the sole cause of the hypotension 
is still undecided. For instance, it may result simply from tachy- 
cardia, for beyond a certain point systolic output falls with an 
increasing pulse rate, owing to insufficient diastolic inflow. 

" Fever will cause rapid heart action by its effect on the accelerans 
nerve endings in the heart. Diminished general pressure results 
in lower cerebral pressure, which of itself stimulates the cerebral 
origin of cardiac sympathetic nerves, especially when the low 
pressure is due to vasoparesis" (Krehl). 

Laryngeal and intestinal complications are often associated with 
low pressures. Arrested cases may show a rise, and relapsing cases 
a tall of tension. Ambulant patients yield higher readings than 
bed-fast cases. 

There are three theories which have been used to explain the 
toxic hypotension of tuberculosis: 

1. That it is due directly and chiefly to the heart muscle, which 
i- pathologically altered, either as the result of the toxins of the 
bacillus or as the result of malnutrition. 

2. That the bloodvessels are primarily the cause of the vaso- 
dilatation, which is the result of the tuberculous toxins. 

1 Nierentuberkulose u, arterielle Hypotension, ZtBchr. f. klin. Mel., L907, Ixii, 358. 



TUBERCULOSIS 225 

.'!. Thai the nervous control of both hearl and bloodvessels is 
essentially influenced by the toxemia, both the vascular dilatation 
and the tachycardia being of nervous origin. 

Two practical facts present themselves: 

First. Is the study of pulse and blood-pressure of prognostic or 
therapeutic value, and is it of diagnostic value previous to the 
time when a diagnosis may be made From physical signs? 

Second. To what is the hypotension due, and to what extent 
can it he remedied by t rent incut ? 

There are wide diversities of opinion on these subjects. Broadly 
speaking, the French writers maintain thai hypotension is a valu- 
able early sign of tuberculosis, which may often be suspected mi 
this account, even when latent; and further, that il i^ a valuable 
differential point in deciding between chlorosis, etc., and incipient 
tuberculosis, also in diagnosticating between tuberculous effusions 
in the pleura and in the peritoneum and non-tuberculous effusions. 

On the other hand, a large number of observers, of wh manj 

arc Germans, find that hypotension is inconstant, and when presenl 
only a late phenomenon. We agree essentially with the latter 
proposition, feeling that the stethoscope is a far better early diag- 
nostic instrument than the sphygmomanometer, believing, how- 
ever, that blood-pressure observations are capable of rendering 
useful data so far as the corroboration of diagnosis, the gauging of 
toxemia, the permitting of exercise, and the recognition of relapses 
are concerned. It is to he home in mind, however, that there is a 
common type of constitutional hypotensive individual who lias a 
low pressure without either active or latent tuberculous disease 
(see Essentia] Hypotension). 

As to the actual causes of tuberculous hypotension, Haven 
Emerson, 1 who has published an excellent clinical and experimental 
study on the subject, arrives at the following conclusions: 

"The causes of low blood-pressure in tuberculosis are probably 
primarily a toxic action on the vasomotor centre in the medulla, 
allowing of a vasoparesis or stimulating an active vasodilatation, 
and, secondarily, progressive cardiac atrophy or degeneration. 
Toxic action on the vasomotor nerves or their motor terminals or 
on the nervous mechanism of the heart cannot be positively denied, 
although there is no proof of it at present. Toxic action of tubercle 
products has not been demonstrated on the muscle of the vessel 
wall or heart, although with regard to the latter, the degenerated 

1 Blood-pressure in Tuberculosis, Arch. Int. Med., 1911, vii (bibliography). 
15 



220 BLOOD-PRESSURE IX < Hh'OXK ' IXFECTIOUS DISEASE 

heart muscle found in advanced eases may have an influence in 
causing hypotension. Rapid heart action is a usual and necessary 
sequel to low blood-pressure, and will, if extreme, aggravate the 
hypotension by the very act of its shortened diastole. It has 
been suggested, but not proved, that lack of vagus inhibition, owing 
to pressure by enlarged bronchial lymph nodes and the presence of 
sympathetic excitation from similar or reflex causes, such as pul- 
monary or gastric irritation, is responsible for the tachycardia 
and hypotension. 

"Hypotension or subnormal blood-pressure is universally found 
in advanced pulmonary tuberculosis, in which condition emaciation 
may be responsible for its causation. 

"Hypotension, when it is present in tuberculosis, increases with 
an extension of the process. Recovery from hypotension accom- 
panies arrest or improvement. Return to a normal pressure is 
commonly found in those who are cured. Continuation of hypo- 
tension seems never to accompany improvement. 

"Displacement of the heart, which is so common a result of 
retracted lung tissue, or loss of expansion due to cavity formation 
or adhesive pleurisy, is spoken of as a cause of tachycardia accom- 
panying hypotension, and it certainly seems to be a contributory 
cause in some cases." 

The question whether hemoptysis is associated with increased 
blood-pressure has received both affirmation and denial. Nor is 
this surprising when we remember that the pressures in the pulmo- 
nary and in the systemic circulation vary independently of each 
other. A progressive diminution of the pulse-pressure indicates 
continued hemorrhage. At the time of actual hemorrhage the 
excitement incidental thereto tends to increase blood-pressure. 
There appears to be no ground to support the contention that 
hemorrhage occurs most frequently in cases with a high systolic 
pressure. The establishment of an artificial pneumothorax is like- 
wise without any constant influence on arterial tension. 1 In one 
of Smith's cases there was a marked unilateral pressure difference 
associated with incomplete collapse of the lung due to pleural 
adhesions. (See Pneumothorax.) 

Blood-pressure estimations have been used as a gauge whereby 
to control exercise in the tuberculous. Peters 2 decreases the amount 
of exercise if ihe patient shows a drop of (> mm. or more after one 

i Smith, !•'. C: The Effed <>f Altitude on Blood-pressure, Jour. Am. Med. Assn., 
nu:,, briv, L812. 

Blood-pressure < lontrol of Exercise in Tuberculosis, < lolorado Med., 1915, vol. xii. 



TUBERCULOSIS 227 

hour's rest, or if exertion is immediately followed by a marked fall 

(10 to 20 mm.) of pressure. 

The Treatment of Pulmonary Hemorrhage. Both clinically and 
experimentally, hemorrhages from the pulmonary vessels tend to 
cease spontaneously, owing to the low blood-pressure in the pul- 
monary circuit and to the reticulated nature of the lung paren- 
chyma. In animals it is difficult to produce a fatal result, even 
when the main branch of a lobe is cut. The protective mechanism 
in man seems to be less efficient. The greal discrepancy which 
exists regarding methods of treatment is due to the fact th.it a 
distinction is not made between the early and late stages of hem- 
orrhage in which the physiological principles in therapeusis are 
radically different. Digitalis, atropin, the nitrites, aconite, chloral, 
chloroform, ergot, adrenalin, pituitrin, and other substances, have 
been recommended. 

We have to consider (1) the effect of the drug on the pub ary 

and (2) on the general arterial blood-pressures; (3) its effect on the 
small pulmonary arterioles; (4) its effed on heart rate and systolic 
output; (5) its effect on the respiratory centre. ( Generally speaking, 
a reduction of pulmonary pressure should reduce hemorrhage, but 
if this is done at the cost of an increased systolic output it will, of 
course, not do so. Constriction of the small pulmonary vessels tends 
to increase pressure in the pulmonary arteries and thus to increase 
bleeding. It is evident, therefore, that the ability to constrict the 
pulmonary vessels is not a criterion of its hemostatic value. The 
maintenance of a normal mean pressure in the pulmonary circuit 
is a function which Nature tends to accomplish in spite of inter- 
ference, just as it does in the case of cerebral anemia. Because we 
lower the systemic pressure, it of course does not follow that we 
lower the pulmonary pressure. Furthermore, in the late stages of 
bleeding, cerebral anemia is prevented by splanchnic vasoconstric- 
tion. To thwart this result might produce death, which is cer- 
tainly a strong argument against the use of the nitrites. What we 
are attempting to accomplish, is to reduce pressure in or reflux 
from the pulmonary vessels without embarrassing the respiratory 
or vasomotor centres or the heart in their efforts to maintain the 
circulation. 

The Physiological Effect of Certain Drugs upon the Pulmonary and 
Systemic Circulations. — Digitalis (without alcohol) produces a rise 
of pulmonary pressure, slight at first, but increasing as its action 
becomes more pronounced. It therefore increases hemorrhage by 
augmenting the systolic output of the right ventricle and constrict- 
ing the pulmonary vessels. 



22s BLOOD PRESSURE TN CHRONIC INFECTIOUS DISEASE 

Ergot primarily decreases pulmonary arterial pressure by depress- 
ing the heart. It is followed, especially in normal animals, by an 
increase due to a secondary augmentation of the beat. Pressure 
in hemorrhage in the pulmonary veins is permanently increased at 
the constriction of the small vessels. The action of the drug wanes 
as the loss of blood continues. 

Pituitrin. —This drug lias been highly recommended by Wiggers, 
since it elevates the systemic arterial pressure through vasocon- 
striction in spite of weakening of the left heart. The decrease in 
amplitude of contraction of the right ventricle causes a fall of pul- 
monary pressure, which neither the weak constricting influence of 
the blood on these vessels nor the backing up of the blood from the 
left heart counteracts. It does not affect the respiratory centre. 
These results occur both in normal and in bleeding animals. 

Chloroform produces a fall of pressure in the pulmonary circuit 
due to depression of the heart and aided by diminished respiration. 
During dyspnea in hemorrhage small doses lessen the respiratory 
movements and so decrease pulmonary pressure and hemorrhage, 
while large doses act similarly through cardiac depression. 

The Nitrites. — In normal-breathing animals a general increase 

in pulmonary pressure is noted, due to increased rate and systolic 

< mtput of the heart. In animals breathing rapidly from hemorrhage, 

nitrites increase both pressure and hemorrhage from pulmonary 

arteries and veins. In the stage in which the nitrites reduce the 

amplitude of respiration a lowering of the pulmonary pressure and 

a reduction of hemorrhage occurs. 

Effect of Various Agents ox Systemic Phkssurk, Respiration, Pulmonary 

Arterial Pressure and Hemorrhage, and Pulmonary Venous 

Pressure and Hemorrhage. (Wiggers.) 









Pulmonary 


Pulmonary 








arterial 


venous 




Systemic 




pressure and 


pressure and 


Drug's. 


pressure. 


Respiral ioi 


hemorrhage. 


hemorrhage. 


Digitalis: 










Normal . . . . 


■ + 


ll 


+ 


(-) + 


Hemorrhage . . . 


. + 





+ 


+ 


Strophantbin: 










Normal \ 
Hemorrhage/ ' ' 


• + 


II 


+ 


+ 


Ergo toxin: 










Normal . . . . 


■ + 


— 


- + 


— 


Hemorrhage . 


(l 


- " 








Pituitary: 










Norm:,! . . . . 


• + 





- <»r (+)- 


— 


Hemorrhage . 


• + 


— 


— 


— 


Chloroform: 










Normal \ 










1 temorrhage/ 










Nitrites: 










Normal . . . . 


— 


I) 


+ 


+ 


Hemorrhages, early , 


- 


+ 


(-) + 


(-) + 


Late . 


— 


- 


— 


- 



PLEURAL EFFl SIONS 229 

It is essential in the treatmenl of hemoptysis, as was shown by 
Wiggers 1 (from whose articles many of the foregoing data were 
taken), to differentiate between the earlj and the late stages of the 
hemorrhagic process. 

Summary. In the early stage of hemorrhage, in a practically 
normal subjecl with only occasional coughing, pulmonarj pressure 
should be reduced by means of cardiac depressants, chloroform, or 
pituitary extract. The nitrites are contra-indicated. In the late 
stages, with tachycardia and tachypnea, the heart and bloodvessels 
no longer react in a typical manner to certain drugs. Cerebral 
anemia manifests itself. The blood supply of the brain mus1 be 
maintained. According to Wiggers, the only drug which can ele- 
vate the systemic pressure and simultaneously lower the pulmonary 
pressure is pituitary extract. 

All clinical and most experimental evidence indicate- that 
morphin is the most valuable drug we possess in the treatmenl of 
hemoptysis. Fear and excitement are among the mosl potenl 
causes of increased arterial tension in general, and probably in the 
pulmonary circulation, and under these condition- nervous sedatives 
are the most rational form of therapy. 

Recent experiments, however, -how that morphin may be harm- 
ful when death is threatened by a hemorrhagic fall of pressure. 
There are two factors to be considered: i 1 i Augmented breathing 
aets favorably from a mechanical point of view in maintaining 
blood-pressure. (2) Excessive breathing may produce acapnia and 
cause a fall of blood-pressure. Wiggers 2 maintains that the former 
condition outweighs the latter in importance, and that morphin 
must be employed with caution. This statement, of course, applies 
only in the case of large hemorrhages in which death is to be feared, 
and the evidence furnished cannot be used to negative the well- 
attested clinical results which have shown the good effects of 
morphin. 

Pleural Effusions. — The existence of pleural and peritoneal effu- 
sions, especially if large, tend to increase blood-pressure, and their 
removal is attended with a fall of arterial tension. The pressure, 
therefore, of such serous effusions may increase a pressure already 
high as the result of nephritis, and a fall of pressure following 
aspiration may not indicate any improvement in the basic condition 



1 A Physiological Investigation of the Treatment of Hemoptysis, Arch. Int. Med., 
July 15, 1911; Studies in Inaccessible Internal Hemorrhages, Ibid., March, 1909. 

2 Wiggers, C. J., Eberly, K. C, and Wenner, H. L.: The Pressor Influence of 

Augmented Breathing, Jour. Exp. Med., 1912, p. 174. 



230 BLOOD-PRESSURE I.\ J CHRONIC IXFECTIOUS DISEASE 

from which the patient suffers. On the other hand, a cardiac 
hydrothorax may cause a pressure sufficiently high to make one 
suspect a coincident nephritis when no such complication exists. 

The emotional disturbance entailed by a prospective operation as 
well as the actual pain of puncture produce a temporary elevation 
of blood-pressure. Aspiration of a pleural exudate is attended by 
a gradual fall of blood-pressure which occurs pari passu with the 
withdrawal of fluid. According to Capps, 1 a fall of 20 mm. is 
usual. The systolic pressure is chiefly affected. This fall of pressure 
is probably not merely the result of the mechanical pressure effects, 
hut is in part due to vasodilator and cardio-inhibitory reflexes. 

After withdrawal there is a gradual rise of pressure, but the 
initial limit may not be reached for some time. The rate of with- 
drawal is no less important than the amount of fluid removed in its 
effect on the immediate fall of pressure. The more long standing 
the effusion the greater the fall of pressure, probably due to imper- 
fect pulmonary expansion. Marked reactions and a slow recovery 
are seen in arteriosclerotic cases. 

By observing the blood-pressure during thoracentesis, untoward 
effects such as weakness, vertigo or collapse, symptoms which 
often occur suddenly and without warning, may be anticipated 
and obviated. (See Aspiration of the Pleura, page 406.) 

Pneumothorax. — Pneumothorax and penetrating wounds of the 
chest, in addition to well-known symptoms, are often associated 
with bradycardia and a rise of blood-pressure (presenting some- 
times an analogy to cerebral injuries), from which signs too opti- 
mistic conclusions may easily be drawn. 

Experimental Data.- — The reports to be found in literature on 
blood-pressure in artificial pneumothorax are very divergent. 
Kakowski- and others report a rise in open pneuniothoraces, 
other investigators no change, and still others a fall of blood- 
pressure. 

According to Walther experimental pneumothorax in the normally 
breathing rabbit is associated with a slowing and an increase in 
the volume of the pulse. Elimination of vagus control does not 
check the rise of pressure which is apparently due to ( \)> stimulation 
of the vasomotor centre. The change in the pulse rate, on the 
other hand, is believed to result from vagus stimulation. The 
difference in response between an open and a closed pneumothorax, 

'Observations on ill" Effecl on the Blood-pressure of Withdrawal of Fluid from 
the Thorax and Abdomen, .lour. Am. Med. Assn., January ">, 1907, xlviii. 
-/in Frage d. Kunstlichen Pneumothorax, Pfluger's Arch., 1910, exxxiv, 31. 



PNEUMOTHORAX 23] 

which is only one of degree, has been explained as due to the facl 
that in the latter, in addition to stimuli which result from pleural 
irritation, those arising in the bronchial mucous membrane (since 
respiratory excursions arc still present) are superadded. The irri- 
tation of the pleura is conducted bj the sensorj fibers of the vagus 
to the nucleus and produces increased vagUS tone. 1 

Clinical Data.- Spontaneous pneumothorax may come on sud- 
denly with acute pain and slunk, especially if the onset occurs 

during exercise in apparently health)- individuals. Frequently, 
however, pneumothorax occurs insidiously- during the course of 
tuberculosis. In the former instance a primary fall of blood- 
pressure is succeeded by a rise to above the normal, which is in 
part at least the result of anxiety, pain, and asphyxia. In the latter 
instance blood-pressure changes are neither constant nor marked, 
especially if only a partial pneumothorax is present. 

There is considerable reason to believe thai the occurrence of 
pneumothorax in the course of tuberculosis may have beneficial 
effects. Certainly the artificial production of this condition is 
often attended with marked symptomatic improvement. Just 
to what extent this is due to changes in the pulmonary circulation 
is as yet uncertain. "It is disputable as to whether the contracted 
lung contains more or less venous blood. In fact, there is experi- 
mental evidence that the pulmonary circulation adapts itself 
promptly to the change and is therefore not particularly disturbed." 3 

The immediate effects of artificial pneumothorax arc variable, but 
once established, the collapsed lung and increased intrathoracic 
pressure have little or no effect upon arterial pressure. 1 The symp- 
toms of shock, and occasionally sudden death have followed this 
procedure. Such events are generally due to a pleural reflex which 
consists of afferent medullary impulses by way of the vagus nerve 
from its terminal filaments, which have been rendered unduly 
susceptible to stimuli as a result of compression or inflammation. 
Death is apparently due to vasoconstriction of the cardiac or 
cerebral vessels. Artificial pneumothorax should never be employed 
in the presence of severe cardiac complications. 5 

1 Walther, H. E.: Zur Kentniss der Puis u. Blutdruckveranderungen beim 
Pneumothorax, Deutsch Ztschr. f. Chir., 1912, cxix, 253. 

2 "Among 500 cases of pneumothorax the onset was sudden in 77 and insidious in 
23 per cent, of the cases. The latter class was evidently underestimated." Pepper, 
O. H. P.: Am. Jour. Med. Sc, October, 1911. 

3 Robinson, S., and Floyd, C: Artificial Pneumothorax as a Treatment of Pul- 
monary Tuberculosis, Arch. Int. Med., 1912, ix, 452. 

4 Smith, F. C: Effects of Altitude on Blood-pressure, Jour. Am. Med. Assn., 
1915, Ixiv, 1812. 

6 Sachs.T. B.: Artificial Pneumothorax in the Treatment of Pulmonary Tuber- 
culosis, Jour. Am. Med. Assn., 1915, lxv, 1S61. 



CHAPTER IX. 

EX( K'.KXOrs INTOXICATIONS. 

Lead Poisoning. The most important exogenous intoxication, 
so far as Mood-pressure is concerned, is lead poisoning. Hyper- 
tension is produced directly as the result of plumbism and indirectly 
as a result of gout, nephritis, or arteriosclerosis, 1 with each of 
which conditions plumbism is closely allied. The onset of both 
lend colic and encephalopathy is associated with marked exacerba- 
tions of pressure even in the absence of nephritis or gross vascular 
lesions. This increase in pressure is believed to be the result of 
vascular spasm, since it disappears after the paroxysm. The arterial 
constriction is evident on examination of the retinal vessels; and 
Pal has reported a case of lead amaurosis which appeared with 
the onset and disappeared with the abeyance of hypertension. 
The systolic pressure is chiefly affected, and large as well as sudden 
variations of pressure are often encountered. Extended observa- 
tions have shown that 80 per cent, of all lead-workers exhibit high 
arterial pressure over years of time even when free from symptoms 
of poisoning, a fact which might be expected if the contention of 
Schmidt, 2 be correct that no real elimination of lead ever occurs, 
once it has entered the body, but merely a transference of it to 
different tissues. Most but not all cases of colic show an exacerba- 
tion of tension coincidently with the colic. The actual pressure 
does not generally exceed 200 mm. Hg., except in cases of enceph- 
alopathy. It seems eminently likely that the pain markedly 
augments the pressure. But that pain is not the essential cause 
is shown by the fact that lowering of pressure relieves it, while 
relief of the pain with morphin does not lower the tension, nor does 
pressure always fall with a spontaneous relief from colic. It has, on 
the other hand, been maintained that the pressure is compensatory, 
and when sufficiently high prevents the colic. The latter view does 
not commend itself. The hypertension has also been attributed 

1 The vascular changes differ from those of ordinary arteriosclerosis. The vessels 
« I c • not collapse and exhibit a normal intima with marked hypertrophy of the media. 
Cardiac hypertrophy is not constant. 

'-' (Jnterauchungen bei experimenteller Bleivergiftung, Deutsch. Arch. I', klin. Med., 
1909, xevi, 587. 



/ / w r<>is<>\ WG 233 

to the effect of lead on the central nervous system. It has also 
been suggested thai the hypertension is due to increased adrenal 
secretion. Heubel ] maintains thai the rise of pressure is purelj 
secondary to nephritis, etc.; while Broadbenl attributes i1 to the 
chemical formation of lead albuminates, which, being with difficulty 
broken down, complicate metabolic changes and render the elimi- 
nation of metabolites difficult. M6netrier and others believe that 
arterial hypertension is a primarj and initial toxic phenomenon. 

Lead colic is generally regarded as due to involvement of the 
solar plexus. Tims, Laignel-Lavastine speaks of the pain, con- 
stipation, and hypertension as symptoms of "solar stimulation." 
Lesions of the ganglia of the plexus have been demonstrated post- 
mortem (Tanquerel, Kussmaul, Maier) and experimentally Mosse). 

Experimental Data. The intravenous injection of lead salts 
produces arterial hypertension. Of course it doe-, not follow 
because acute intoxication produces this effect that therefore 
chronic poisoning will have similar results. The chief physiological 
action of lead is exerted on striated muscle, in which it produces a 
diminished functionation (Nothnagel and Rossbach). This would 
lead to vasomotor relaxation and, unless it were counter-balanced 
by compensatory vasoconstriction, to a fall of pressure. According 
to Jores, 2 such a relaxation occurs in the smaller arteries of rabbits 
poisoned with lead. 

Clinical Data. — Hypertension has long been observed clinically. 
The presence of hypertension, especially if nephritis can be elimi- 
nated, should certainly suggest the possibility of plumbism even if 
the gingival blue line or basophilic degeneration of the erythrocytes 
cannot be demonstrated. Arterial stasis alone will not increase 
pressure, and since there is a marked hypertension during attacks 
of colic, we must assume a vasoconstriction, either as the result of 
a toxic effect or owing to some compensatory antagonistic physio- 
logical action (central vasoconstriction?). 

Furthermore, as shown by Hasebroek, the sphygmograph of a 
lead pulse is more like that of a normal pulse than that of an arterial 
hypertension. He uses this and some of the foregoing arguments 
to establish the existence of an active arterial diastole, and believes 
that plumbic hypertension results not from vascular spasm but from 
an "increased activity of the pressor components of physiological 
vascular functionation." Stewart in his studies on blood flow found 

1 Path. u. Sympt. der chr. Bleivergiftung, Berlin. 

2 Ueber die path. Anat. d. chronischen Bleivergiftung des Kaninehens, Aliinehen. 
med. Wchnschr., 1902, p. 713. 



234 EXOGENOUS INTOXICATIONS 

in lead poisoning without paralysis a conspicuous tendency to reflex 
vasoconstriction. 

Well-marked bradycardia is quite common. In 1179 cases Tan- 
querel found the pulse rate between 20 and 00 in 678, between 
65 and 70 in •">7(i, and between SO and 100 in 125 cases. Such cases 
are a true bradycardia due, it appears, to a toxic effect upon the 
vagus nerve or its terminations. The bradycardia and the arterial 
hypertension are independent phenomena. 1 

Encephalopathy. — In this condition very high pressures are often 
encountered. Menetrier- attributes the symptoms to the high 
pressure. 

In a man, aged twenty-one years, during one of many attacks 
of colic, a pressure of 260 mm. was found which soon reached 300 
nun. and was then associated with marked cerebral symptoms. 
At autopsy the kidneys were normal, as had been the urinary find- 
ings during life. The brain showed marked signs of pressure, 
edema, distended membranes, flattened convolutions, etc. 

It appears, therefore, that plumbism may be accompanied by 
numerous clinical manifestations which strongly suggest vascular 
spasm as the basis of their production. Thus the abdominal colic, 
anginoid attacks, encephalopathy, including amaurosis, hemianopia, 
aphasia, deafness, etc., have been attributed to local vascular 
contraction. 

Although generally associated there is no absolute parallelism 
between pain and vascular spasm; either may exist without the 
other. It is not yet proved that lead colic is due (1) to spasm of 
intestines or to (2) spasm of mesenteric arteries. It is apparently 
associated with a general vascular spasm in which, of course, the 
splanchnics have a part. Such a general contraction may begin 
suddenly or gradually, hence it is often difficult to say what the 
individual's normal is. The fact that pain is absent is no proof that 
the vessels are not contracted. Hypotension (55 to 75 mm. Hg.) 
may follow colicky attacks. Relief from constipation often goes 
hand in hand with the disappearance of pain and with a fall of 
pressure (IJiegel). 

With so many divergent theories and such equivocal experi- 
mental and clinical findings, we must conclude by saying that 
although in lead poisoning •hypertension is constant, and exacer- 
bations of tension frequent, we are still unable to make positive 
statement as to the exact mechanism by virtue of which these 

i Lion :ind Marcorelles: Presse Med., 1913, No. 12, p. 109. 
Soc. med. iles Edpitaux, February 12, mill. 



TOBACCO 235 

vascular phenomena are produced, or whether thej are primary or 
secondary manifestations. Persistent marked hypertension is of 

bad augury in plumbism. Borgen has ohser\ ed the following 
phenomena in cases of lead colic: I I I period of rising pressure, of 
variable duration; (2) period "I' high pressure, one to torn- days; 
either of the above may be associated with colic; '■'< period of 
decrease, two to four days, with disappearance of symptoms; I 
period of subnormal pressure (95 mm.). 

Therapeutics. If the c :eption of the pathological proces a a 

local (or general) vascular spasm i^ correel then purgation with 
salines and belladonna is a rational procedure. The administrates 
of morphin is purely palliative. Pal endorses the custom sanc- 
tioned- administration of the iodides in large doses saying that 
symptoms of lead colic eease as soon as those of iodism appear. 
Some researches have thrown doubt upon the efficacy of the iodides, 
at least so far as elimination is concerned, and have suggested the 
employment of bile salts. The administration of the nitrites in 
large doses (■£-$ gr. nitroglycerin hourly) sometimes alleviates the 
pain of lead colic promptly and permanently. I have observed this 
fact on numerous occasions. 

Phosphorus. — Acute phosphorus poisoning so far as the cir- 
culation is concerned, produces a degeneration of the heart muxle, 
and while this is doubtless a contributing factor in the cause of 
death, it appears from Pahs investigations that the primary cause 
lies in a fall of blood-pressure due to loss of vasomotor tone. 

Chlorin Gas. — The inhalation of chlorin gas which has been \\-i-<\ 
in trench warfare causes a marked fall in blood-pressure, a slow inl- 
and irregularity of respiration and pulmonary symptoms which are 
apparently due to obstruction of the pulmonary circulation rather 
than to spasm occlusion of the bronchioles. 1 

Arsenic. — Acute arsenical poisoning causes a fall of blood-pressure 
due to depression of the heart and the vasomotor centre. • 

Tobacco. — There has been much discussion as to whether the 
constitutional effects which follow the use of tobacco are due to 
nicotin or to other substances. The evidence at hand indicates 
that nicotin is by far the most important, if not the sole factor, 
but other substances, such as carbon monoxid, hydrocyanic acid, 
furfural and other aldehyds, have also to be reckoned with. 

Lehman has shown that the slower the rate of smoking the smaller 
the amount of hydrocyanic acid formed. This substance, however, 
seems to be present in too small amounts to account for physio- 

1 Schafer, E.: On the Immediate Effects of the Inhalation of Chlorin Gas, British 
Med. Jour., August 14, 1915, p. 245. 



236 EXOGENOUS INTOXICATIONS 

logical symptoms. The ordinary cheap cigarettes (Virginia tobacco) 
contain only a negligible quantity of nicotin. They do, however, 
contain a large quantity of furfural to which the harmful effects 
may be due, yet this substance is practically absent from Turkish 
cigarettes. 1 

Experimental Data.- With moderate quantities of nicotin the 
pulse rate is slowed; the heart may stop for a few seconds in diastole, 
then gradually assume an accelerated rhythm. The slowing is due 
to stimulation of the vagus ganglia. "It is not affected by section 
of the cervical pneumogastric, as the path from the ganglia to the 
cardiac ganglia is still intact, but, on the other hand, it is prevented 
by atropin, which acts on the extreme terminations of the inhibitory 
fillers, and therefore blocks the passages of impulses from the 
ganglia to the muscle." 

Nicotin is second only to epinephrin as a vasoconstrictor. Blood- 
pressure is increased owing partly to stimulation of the vasocon- 
strictor centre in the medulla, but chiefly to peripheral influences, 
for it occurs even after extirpation of the spinal cord. " The vaso- 
constrictor nerves pass through ganglia on their way to the vessels, 
and the rise of blood-pressure seems to be mainly caused by a stim- 
ulation of these ganglia" (Cushny). Hemorrhage causes a marked 
increase in the vasomotor reaction to nicotin. 2 

The fact that on analysis a certain variety of tobacco is shown 
to contain a greater or a smaller quantity of nicotin by no means 
proves that when smoked it will yield an equivalent amount. In 
fact, the very opposite result may be obtained. The nicotin content 
of the smoke depends largely on the completeness and quickness of 
combustion. Ordinarily, half of the nicotin is destroyed by com- 
bustion. Of the remainder variable quantities reach the mouth, 
being carried there by the hot smoke, which, in passing through the 
condensation area, volatilizes certain substances in the tobacco. 
Hence the larger the condensation area (long, thick cigars) the 
greater the amount of nicotin, etc., which comes through. 

The smoking of tobacco in the form of cigarettes is, for an equal 
amount of this substance consumed, less harmful than when used 
in the form of cigars or a pipe, assuming of course that inhalation 
is practised in each instance, because of the more complete combus- 
tion which ensues. Long cigars are relatively more injurious than 
short ones because they furnish a large condensation area in which 
the un consumed nicotin accumulates. The last third of the cigar 
is therefore more toxic than the first two-thirds. For the same 

i Sec- editorial, Jour, Am. Med. Assn., 1912, lix, 1798. 
Boskins, Rowley and Roeser: Arch. Int. Med., 1915, xvi, 466. 



TOBACCO 237 

reason a cigar which bas ceased to burn should not be relighted. 1 
The habit of holding an extinguished cigar between the lips should 
not be practised. Long-stemmed pipes are better than shorl ones. 

Tobacco and Arteriosclerosis.- The importance of tobacco as an 
etiological factor in arteriosclerosis has been much discussed and 
the question still remains unsettled. The tobacco babil is usually 
coupled with the use of alcohol and frequently with faulty methods 
of living. It lias yet to be shown thai the career of smokers is 
shorter than that of non-smokers. It is admitted that tobacco is a 
cardiovascular poison which is at first an excitant to the neuro- 
muscular apparatus, later a motor nerve depressant, and finalh a 
paralyzant of the cardiac nerves. But whether it produces arterio- 
sclerosis, either by its direct toxic action on the vessels or indireel ly 
by its effect on blood-pressure, is a very differenl question. Lee 
apparently succeeded in producing definite vascular lesions in 
rabbits which were made to inhale tobacco smoke over prolonged 
periods of time. 

Clinical Data.- There are of course individual differences, but 
generally tobacco tends to raise both the pulse rate and the blood- 
pressure, the former being in part the cause of the latter. These 
effects often appear after the first inhalation of smoke, and may be 
accompanied by a sensation of nervousness and sometimes pre- 
cordial fulness or palpitation. The secretion of the adrenals is 
controlled by the sympathetic nerve, which is at first stimulated 
and later depressed by the administration of nicotin. 2 

The elevation of blood-pressure ranges between 3 and 25 mm., 
the systolic pressure being chiefly affected, indicating that the heart 
is more affected than the bloodvessels. Pressure generally falls to 
or slightly below the original level within twenty minutes. Hesse 3 
found these results more marked in smokers than in non-smokers. 
The greatest rise in the pulse rate was twenty-five beats per minute. 
A return to the normal occurs in from twenty to fort}' minutes. 
Excessive quantities of nicotin cause a fall of pressure from depres- 
sion of the vasomotor centre and may in this way actually cause 
collapse. Strong tobacco causes more marked effects than the 
weaker varieties and in strongly reacting individuals the pressure 
may remain high for two hours. 4 Acute tobacco poisoning causes 

1 Lee, W. E. : The Action of Tobacco Smoke, with Special Reference to" Arterial 
Pressure and Degeneration, Quart. Jour. Physiol., 1908, p. 335. 

2 Cannon, Aub, and Binger: A Note on the Effect of Nicotin Injection on Adrenal 
Secretion, Jour. Phar. and Exp. Therap., 1912, iii, 379. 

3 Deutsch. Arch. f. klin. Med., March 15, 1907. 

4 John, M.: Ueber d. Beeinflussung des systolischen u. diastolischen Blutdrucks 
durch Tabakrauchen, Ztschr. f. exp. Path. u. Therap., 1913, xiv, 352. 



238 EXOGENOUS INTOXICATIONS 

a fall of blood-pressure, associated with nausea, vomiting, vertigo, 
and sudation. 

Tobacco, then, should he forbidden, or its consumption limited 
when (1) ve wish to spare the heart — cardiac, renal, pulmonary 
disease, etc.; (2) in arterial hypertension; (3) in arteriosclerosis. 

Chronic Alcoholism. — Chronic alcoholism is associated with 
variable blood-pressure, depending upon the extent to which renal 
and cardiovascular changes have occurred. But alcoholics in whom 
these organs are sound, show, when abstinence has been enforced, 
a marked rise of the systolic pressure followed after a few days by a 
gradual fall. The diastolic pressure is constantly high. Raff 1 finds 
these results so constantly as to be of diagnostic value in differen- 
tiating between alcoholism and functional neuroses. 

Delirium Tremens. — In the asthenic type of case the systolic 
pressure is uniformly low and the pulse-pressure small. A reestab- 
lishment of normal relations goes hand in hand with the subsidence 
of delirium. r I Tiis would indicate that the height of blood-pressure, 
through its effect on the cerebral circulation, bears a causal relation 
to the delirium, a statement which is further borne out by the fact 
that if more normal values can be temporarily established by what- 
ever means, symptomatic improvement occurs (Pettey). 2 The 
treatment of delirium tremens by means of lumbar puncture has 
been attended by excellent results. It appears that the delirium 
is in part due to increased cerebrospinal pressure, and in part to 
toxicity of the spinal fluid. As pointed out elsewhere there is no 
constant relationship between arterial and cerebrospinal pressure. 
(See Meningitis, and Lumbar Puncture.) 

Hogan 3 in 53 cases of delirium tremens has reported systolic 
pressures ranging from 95 to 220, the average being 140. These 
eases were treated by the intravenous administration of hypertonic 
alkali and also glucose dissolved in water and given in large infu- 
sions, lie found despite the large amount of fluid infused and its 
alkaline character blood-pressure was reduced in the high-pressure 
cases. The rationale of this treatment, which appears to have been 
attended with a marked amelioration of symptoms, is that the hyper- 
tonic solution dehydrates the body colloids and diminishes edema 
of the brain as well as of the other tissues. 4 

1 Blutdruckmessungen bei Alkoholikern u. funktioneilen neurosen unter Ausschlusa 
von Kreislaufstdrungen, Deutsch. Arch. f. klin. Med., 1913, oxii, 209. 

•The Narcotic Drug Diseases and Allied Ailments, Philadelphia, 1913, p. 99. 
Treatmenl <>f Acute Alcoholic Delirium, Jour. Am. Med. Asso., 1916, lxvii, 1826. 

4 In the preparation "t the solutions 5.8 gms. of chemically pure sodium chloride 
and 8. t gms. <>f chemically pure sodium bicarbonate are boiled in 120 c.c. of distilled 
water and filtered through paper, then placed in :i Bask and reboiled. In addition 
Hi. J gms. "I chemically pure Bodium bromide is boiled in :■!(> c.c. distilled water, 
filtered and reboiled. These may be kept ready fur use, and when needed are 



CARBON MONOXIDE P0IS0N1M, L':;'.) 

Morphinism. -According 1<> Pettey, rphin habitues general!} 

show ;i high pressure due largely, it seems, t<> portal conge tion, 

since evacuation of the bowels often causes a fall of from ."ill to 6Q 

nun. Hg. "This reduction of arterial tension by the preparatory 
treatment, now universally verified, is an essential factor in pre- 
venting collapse and other dangerous complications during the 
withdrawal period." 

Patients admitted with a blood-pressure of L80 to 200 nun. were 
usually found to have a Mood-pressure of 1 Hi to L50 after the sys- 
tem had been cleansed of toxic matter and the drug withdrawn. 
The lowered record is maintained throughout convalescence, show- 
ing that it was the individual's normal pressure. 

The experience of the writer with this class of patients has been 
limited, but he nevertheless feels that the preceding statements 
must be accepted with reserve. Certainly, patients with 'he opium 
habit as seen in our hospitals arc generally admitted in a condition 
of scmicollapse, due to starvation, intoxication, and cachexia, with 
blood-pressure distinctly below the normal. 

Yalenti 1 found that if morphin were withdrawn from dogs which 
had become accustomed to its use, marked circulatory disturbances 
such as arterial hypotension, arrhythmia and tachycardia occurred. 
These symptoms abated if the use of the drug was renewed. 
Furthermore, the serum of dogs suddenly deprived of morphin 
caused similar symptoms when injected into other dogs, whereas 
the serum of unmorphinized dogs has no such effect. It seems 
evident, therefore, that during the withdrawal stage, circulation 
stimulation may be necessary. 

Carbon Monoxide Poisoning. — In the early stages of ( '( ) poisoning 
blood-pressure rises, the pulse rate is increased and not infre- 
quently irregular. Later blood-pressure falls and the cardiac rate 
alternates between bradycardia and tachycardia. Finally, in the 
third stage, with a weak, thready pulse, and a leaky skin, blood- 
pressure falls owing to paralysis of the vasomotor centre. 2 



added to 850 c.c. of either freshly distilled water or tap water that has been filtered 
and boiled. .Under no circumstances should old distilled water be used, as it may pro- 
duce severe chills. This mixture is heated to about 110° F. and is ready for use. 

In a flask with 250 c.c. distilled water 80 gms. of glucose are placed and boiled. 
To this is added 0.25 gm. of blood charcoal. This is allowed to stand for twenty- 
four hours, is then filtered into a clean flask, reboiled, and is ready for use. This 
solution may be made up and kept ready for use. 

Both of these solutions must be given very slowly, from twenty to thirty minutes 
being taken for the 1250 c.c. 

1 Experimentelle Untersuchungen u. d. chronischen Morphinismus, etc., Arch. f. 
exper. Path. u. Pharmakol., 1914, lxxv, 437. 

2 Glaister and Logan: Gas Poisoning in Mining and Other Industries, Edinburgh, 
1914, p. 207. 



CHAPTER X. 
BLOOD PRESSURE IX CARDIAC DISEASE, Etc. 

Mechanical Hypotension. When the total volume of blood is 
diminished from whatever cause (hemorrhage, diarrhea, sweating, 
polyuria) a fall of blood-pressure may result. Eor a time, of course, 
this may be counter-balanced by arterial constriction. Such a hypo- 
tension is seen typically in postpartum hemorrhages. Whether 
the hypotension seen in severe anemias, often with a diminished 
viscosity, has a similar genesis cannot be positively asserted. 

Factors which hinder the flow of blood to or from the right heart 
(a fall of venous pressure, adhesive or effusive pericarditis, obstruc- 
tion in the pulmonary circuit, portal or caval obstruction, etc.) 
produce arterial hypotension. The removal of serous effusions from 
the peritoneum or pleura tends to produce a similar effect, as do 
also cardiac and valvular lesions in the stage of broken compen- 
sation. 

Functional Hypotension. — This form of hypotension occurs when 
vascular tone, especially in the splanchnic vessels, is below the 
normal or when a local vasodilatation is insufficiently compensated 
for by local constriction elsewhere. It is seen chiefly in fevers 
(toxemia), in constitutional low arterial tension, and in medical or 
surgical shock. 

Terminal Hypotension. — Terminal hypotension may result either 
from mechanical or functional causes. By this term we mean the 
ultimate fall of pressure which occurs as a result of cardiovascular 
failure. It is seen in the agonal and preagonal periods. It is com- 
mon as the terminal stage of hypertension, in which the pressure 
may be only relatively, not actually, below the normal. Occasion- 
ally life may be maintained for several hours or even days with a 
max in i nn i pressure of 60 mm. Ilg.; indeed, figures as low as 45 mm. 
(associated with unconsciousness and a subnormal temperature) 
have been reported by Neu. 

Diseases of the Heart. Despite the great abnormalities of the 
circulation, which arc manifest during the course of valvular and 
myocardial disease, pressure observations often show relatively 
insignificant changes. Increased blood-pressure is essentially a vas- 
cular and myocardial, not a valvular phenomenon. Excluding the 



DISEASES <>F THE HEART 241 

conspicuous findings of aortic insufficiency and cardiorena) hyper- 
tension, sphygmomanometric readings often arc of discouragingly 

little clinical value, although a normal systolic, associated with a 
high diastolic, pressure is very suggestive of myocardial disease. 
This is due to the fact that although the general systemic pressure 
may he normal, the rapidity of blood flow, the mass movemenl of 
the blood, and especially the normal pressure relations between the 
arteries, arterioles, capillaries and veins have been either locally 
or generally disturbed. Regarding these conditions ordinary 
sphygmomanometric observations teach us but little l>\ inference 
and nothing directly. 

In valvular disease one frequently finds diminished pressure, 
100 to 110 mm., but such a hypotension is more often attributable 
to coincident conditions, such as fever, etc., than to a direct cardiac 
effect. In acute rheumatic endocarditis the pressure is not different 
from that in old valvular lesions. Rarely blood-pressure and tem- 
perature rise and fall together. Only exceptionally does the pressure 
in afebrile cases fall below 90. Not infrequently pressure values, 
remain the same in broken compensation and during subsequent 
improvement. Digitalis produces practically no rise of pressure in 
valvular cases. In cardiac decompensation it tends to increase the 
pulse-pressure rather by lowering the diastolic, than by elevating 
the systolic, pressure. 

We may have a stasis of blood due to increased resistance in the 
peripheral arteries without elevation of either the systolic or the 
diastolic pressure. The condition which Sahli has described as high- 
pressure stasis ("hochdruckstauung") occurs when the arterioles 
are tonically contracted or sclerotic so that outflow is prevented. 
Under such circumstances even an insufficient heart may, by forc- 
ing gradually more blood into the arterial reservoir, increase the 
pressure. This is further abetted by the accumulation of C0 2 in 
the blood, which, by stimulating the vasomotor centre, leads to 
still further arterial contraction. 

In these cases a plethoric, cyanotic face is often associated with 
edema and other evidences of cardiac failure, together with high 
arterial tension, which falls when circulatory improvement occurs. 
This is attributable to improved renal elimination, to a diminu- 
tion of carbon dioxide tension in the blood and to lessened hydremic 
plethora (see p. 276). A fall of pressure is of serious import chiefly 
when associated with a rise of venous pressure, the latter being 
manifested by hepatic and pulmonary congestion. Vascular reflexes 
are sometimes abolished in advanced cardiac disease. 
16 



242 BLOOD-PRESSURE TN CARDIAC DISEASE 

Aortic Insufficiency. — Experimental Data. — The establishment of 
experimental aortic insufficiency in animals, insofar as concerns 
the mean arterial pressure, has shown divergent results. Some 
investigators have reported a fall of the mean pressure; others but 
little change. The results seem to depend, at least in part, upon 
the cardiac strength of the animal in question — dogs hearing the 
lesion better than rabbits. As a rule there is some fall of the mean 
pressure, the amount of which tends to vary with the duration and 
severity of the lesion. 

The arterial pressure is perhaps maintained in suddenly estab- 
lished aortic lesions by the vasomotor and cardiac reflexes which 
are engendered by stimulation of the endocardium, but the chief 
factor of compensation lies in the heart muscle itself. The mean 
pressure is maintained chiefly as the result of enlargement and 
hypertrophy of the left ventricle, which lead to an increased systolic 
output. 1 

The experiments of Stewart 2 indicate that much less blood actu- 
ally regurgitates into the heart during diastole than is generally 
supposed. This is owing to the increased tonicity which the left 
ventricle assumes. The great difference between the systolic and 
the diastolic pressure which occurs has been attributed to a reflex 
lowering of the minimum pressure. The main fall of pressure is 
systolic in time, and is due to increased capillary flow. This is borne 
out by the fact that even in case of good compensation the diastolic 
pressure may range between 40 and 60 mm. Ilg., while the systolic 
pressure is about 180 mm. The tremendous pressure fluctuations 
to which the arteries are subjected is an important factor in the 
arteriosclerotic changes which the vessels undergo in these cases. 

Wiggers's 3 studies with optical manometers, however, indicate 
that the rapid systolic fall of pressure is not due to vasodilatation, 
since (1) the change occurs too rapidly (within a single beat), (2) 
it occurs even when the vessels have been previously dilated by 
means of nitroglycerin, and (3) the condition is enhanced rather 
than abated by epinephrin. 

lie attributes the dynamic changes of aortic insufficiency to the 
fact that the initial intraventricular tension is increased "owing to 
a regurgitation of pressure during diastole; this in turn causes a 
more vigorous ejection of a larger blood volume in the early portion 
of the next systole. This may be accompanied by an actual 

1 Krehl, L.: Pathologische Physiologic, L910, p. is. 
Experimental and Clinical Envestigations of the Pulse and Blood-pressure changes 
in Aortic Insufficiency, Arch. Int. Med., 1908, i, L02. 

The Dynamics of Aortic Insufficiency, Arch. Int. Med., 1915, \\i, 132. 



I <//,•/ i, TNSl FFICIENCY 243 

decreased ejection during the hitter portion of systole, thus al 
once accounting for the facts (a) thai the systolic dr. -line becomes 
steeper and (6) that the total systolic output may no1 increase 
appreciably beyond the normal." 

Clinical Data.- The enormous pulse-pressure \\ hich in exceptional 
cases may amount to L20 mm. Hg. and which is frequently seen in 
aortic insufficiency with good compensation is often sufficient to 
alone establish a diagnosis. This finding i^ analogous to the other 
pulsatory phenomena which are so characteristic of this lesion. 

l.andolfi, Koch, and others have reported circulatory hippus as a 
sign. It is generally manifest when the pulse is slow and the systole 
powerful (digitalis). Myosis corresponds with systole or increased 
pressure. 

A high systolic (180 to 200 mm.) associated with a low diastolic 
(60 to 30 mm.) pressure is strong presumptive evidence in favor 
of aortic regurgitation. In estimating the diastolic pressure by the 
auscultatory method the fourth phase must be chosen as the cri- 
terion, since the fifth phase often persists down to mm. This 
phenomenon is suggestive but not pathognomonic of aortic insuffi- 
ciency. A fall of pressure often indicates a failing ventricle. We 
should not speak of hypertension in cases of aortic insufficiency 
unless the systolic pressure exceeds 200 nun. 

The intensity of the diastolic aortic murmur in some cases 
increases with a rise of systolic pressure. A fall of pressure may 
cause a feeble murmur to become inaudible. The arterial sound 
heard in some cases in the femoral artery without aortic leakage 
depends to a considerable extent upon the pulse-pressure, but 
especially upon the existence of an abnormally low diastolic pressure 
(Dehio).' 

Differences in the Blood-pressure in the Arm and Leg. — Under 
normal conditions the systolic pressures in the arm and leg of an 
individual lying quietly in a horizontal position are equal. When 
the erect or an inverted posture is assumed the pressures in the 
arm and leg "differ by the hydrostatic pressure of the column of 
blood which separates the points of the measurements. In these 
postures the pressure in the arteries of the leg varies greatly, while 
in the arm the pressure is kept about the same by the mechanism 
which compensates for the influence of gravity." In aortic insuffi- 
ciency a great difference between the arm and leg pressures in the 
recumbent posture has been found (150 mm. Hg. higher in the leg) 
which is of diagnostic significance. It is most marked in uncompli- 
cated and compensated cases and diminishes as soon as mitral 



244 BLOOD-PRESSURE IN CARDIAC DISEASE 

insufficiency and dilatation of the right heart occur. Both fever 
and the application of hot water lessen the difference by relaxing 
arterial tone in the lower extremities, 1 in which the arteries are 
assumed to he in a contracted state in an effort to prevent cerebral 
anemia.'-' Another explanation of the higher leg pressure is offered 
by Hill and Wells 8 who believe that it is due to a better conduction 
of the pulse wave in contracted and more rigid arteries. Hill 4 
has recently stated that in addition to the just mentioned factors 
the resonating effect (periodic vibration) of the abdominal cavity 
also plays a part. According to the latter conception " Resonation 
of the tissues must be held to play an important part in the trans- 
mission of the pulse, and thereby to save the work of the heart. 
The work of the heart we know is largely conserved by the elastic 
recoil of the arteries. But this elastic recoil of the arteries is aided 
by the resonance of the tissues. Every artery is in intimate relation- 
ship with its immediate neighbor. The pulse of one individual 
artery is aided by the pulses of the other arteries. The vigor of 
the circulation depends on the tone of the tissues, on the tautness 
of skin and muscle, and particularly of the abdominal wall. The 
hardened body of the trained athlete swings in full resonance with 
the pulse of his heart; the soft, flabby, ill-conditioned body of the 
sedentary worker offers a poor slack drum for his' heart to thump." 

Cases Illustrating the Differences in Arm and Leg Pressures in Aortic 
Insufficiency as Compared with Other Cardiac Lesions. 

Blood-pressure 
Brachial. Ext. malleolar. 

No. 1 Hagnosis. Systolic. Diastolic. Systolic. Diastolic. 

1 Arteriosclerosis, chronic nephritis, car- 

diac hypertrophyand dilatation.em- 

physema of lungs, portal congestion 171 106 167 107 

2 Mitral and tricuspid insufficiency, car- 

diac dilatation, passive congestion of 

lungs, liver, kidneys, portal system 113 75 112 80 

:; Aortic obstruction and insufficiency, 
arteriosclerosis, mitral insufficiency 
cardiac hypertrophy, etc. . . . 151 69 191 122 

4 Aortic obstruction and insufficiency 

initial insufficiency, arteriosclerosis, 

chronic nephritis, etc 173 71 190 95 

5 Cardiac hypertrophy and dilatation, 

aortic insufficiency 222 127 300 190 

1 Rolleston, 11. I'.: I >n the Systolic Blood-pressure in the Arm and Lou in Aortic 
Incompetence, Heart , 1912, iv, >•■:. 

Hill. Flack, and Holzman: The Measurement of Systolic Blood-pressure in Man, 
Heart, 1909, i, 73. Hill and Rowlands: Systolic Blood-pressure, Heart, 1912, iii, 
219. 

Wells, Russell, and Hill: Roy. Sue. Proc, 1913, B. lxxxvi, 180. Hill and Flack: 
ibid., p. 365. 

4 Hill. McQueen, and Ingram: The Resonance of the Tissues as a Factor in the 
Transmission of the Pulse and in Blood-pressure, Proc. Roy. Soc, London, 1914, 
lxxxvii, 255. 



AORTIC ANEURYSM 245 

In Cases 1 and 2 there \\ as n<> aortic leakage. The arm and leg 
pressures in the recumbent position were approximately equal. In 
Cases 3 ;iml 4 (definite aortic insufficiency) there were marked 
differences in pressure. In Case 5 aortic regurgitation was doubt- 
ful but the large pulse pressure, as well as the arm and leg differ- 
ence, were strong evidence in favor of the existence of the lesion. 

The difference in the arm and leg pressures jusl referred to, while 
suggestive and corroborative, are not pathognomonic of aortic 
insufficiency. They, as well as a large pulse-pressure, are met with 
in arteriosclerosis. 1 

Traube's Sign a double torn heard over the femoral ves els 
oeetii's chiefly in aortic insufficiency, as does also Duroziez's sign a 
double murmur heard as the result of stethoscopic compression of 
the femoral artery. Both of these phenomena are mosl marked 
when the pulse-pressure is large. The former is caused by sudden 
distention of the artery by the large systolic output and by the 
sudden distention of the femoral vein due to tricuspid insufficiency. 2 

Iluchard found that in aortic insufficiency of rheumatic origin 
the systolic pressure was increased only moderately; the diastolic 
pressure was subnormal; while in cases of arteriosclerotic <>ruj'<u both 
phases were markedly elevated. These findings he attributed to 
the greater valvular damage in Group I and the coincident presence 
of renal lesions in Group 2. 3 

Aortic Obstruction. — In pure aortic obstruction the systolic the 
diastolic and the pulse-pressures are generally slightly elevated, 
due in part to left ventricular hypertrophy and in part to general 
arteriosclerotic changes. The pulse-pressure is small, and the pulse 
feels hard and small, being gradual both in onset and in disap- 
pearance. 

Aortic Aneurysm. — Many cases of aortic aneurysm have a normal 
arterial pressure. According to Williamson, 4 blood-pressure tends 
to be higher in cases of simple aortic dilatation than in cases in 
which a distinct aneurysm is present. A pressure difference (5 to 
20 mm.) in the two arms is very commonly found, and occurs in 
about the same proportion of cases whether the innominate artery 
is actually involved or not. Differences amounting to 30 mm. or 

1 Taussig, A. E. : Some Blood-pressure Phenomena in Exophthalmic Goitre, Tr. 
Assn. Am. Phys., 1916, xxxi, 121. 

2 Schultz, W. : Ueber d. Doppeltonbildung a. d. Cruralgefaessen, Deutsch. med. 
Wchnschr., 1905, xxxi, 2, 13S1. Tice, T.: Clinical Significance of Some Peripheral 
Signs of Aortic Insufficiency, Illinois Med. Jour., September, 1911. 

3 Huchard, H., and Amblard: La tension arterielle dans les insuffisances aortiques, 
Jour, de Practiciens, May 29, 1909. 

4 Lancet, November 30, 1907. 



246 BLOOD-PRESSURE IX CARDIAC DISEASE 

more occur in about one-third of the cases and indicate aneurysm 
rather than simple dilatation or mediastinal tumor, which latter 
causes inequality of tension somewhat less frequently than does 
aneurysm. Small inequalities of pressure are of little practical 
diagnostic value. Unilateral differences of 10 mm. in the two arms 
without any constancy as to the side occurred in 20 per cent, of 
36 cases studied by Phipps. 1 The administration of potassium 
iodide or the injection of sterilized gelatin, which often relieves 
pain, has no effect on arterial tension. 2 

Unilateral pressure differences may also be encountered in arterio- 
sclerosis, in hemiplegia, and in cases of cervical rib. In the last- 
named condition lowering of the arm sometimes produces a demon- 
strable decrease in the pulse-pressure. 

Increased blood-pressure, especially that which is due to sudden 
muscular strain is, next to disease of the elastic fibers of the arterial 
media, the most important factor in the production of an aneu^sm. 

Phlebotomy which is often a very useful method of therapeusis 
in aneurysm, lowers blood-pressure, and if the blood withdrawn has 
been considerable in quantity — one pint or more — the patients are 
often symptomatic-ally benefited for weeks op months. 

Subclavian Aneurysm. — Dilatation or aneurysm of the subclavian 
artery has been reported in a number of instances as a result of 
pressure upon the artery by cervical ribs. The vascular abnormality 
occurs distal to the site of pressure. The mechanism by which dila- 
tation occurs has been investigated by Ried 3 who found that if the 
canine abdominal aorta is partially occluded by a metallic band, 
the systolic pressure in this vessel falls, while the diastolic pressure 
ti~'->. Based upon the foregoing experiments Ilalstead believes that 
the subclavian dilatation is not a result of vasomotor paralysis, 
trauma or sudden variations in blood-pressure, but is due to the 
abnormal whirlpool-like play of the blood in the relatively dead 
pocket just below the site of the constriction and the lower pulse- 
pressure. 

Mitral Lesions. -In compensated mitral insufficiency arterial 
pressure is practically normal. The reestablishment of functional 
efficiency after an attack of broken compensation is, as was first 
pointed out by Sahli, not rarely associated with a diminution of 
blood-pressure. In mitral lesions this rule applies to both maximum 

' Boston Med. and Surg. Jour., L915, clxxiii, 47G. 

- Mackinnon, M.: Arterial Pressure in Thoracic Aneurysms, British Med. Jour., 
October I. L913. 
:: Partial Occlusion "I the tarta with the Metallic Band. Observations on Blood- 
res and Changes in the Arterial Walls, Jour. Exper. Med., L916, xxiv, 287. 



Mill; \i. LESIONS 



247 



and minimum pressures. The same phenomena occur to an even 
greater extent in the broken compensation which occurs in pul- 
monary emphysema. In aortic and arteriosclerotic lesions the fall 
of pressure is much less marked. These apparently paradoxical 
phenomena are due to the fact that during the period of insuffi- 
ciency the resistance to arterial outflow is increased as the resull 
of (1) CO2 accumulation in the blood which produces peripheral 
vasoconstriction, and (2) owing to increased venous pressure. The 
physics of this phei Lena are illustrated in the toll., win- diagram: 





M 
A 




a 


— in 








u u 



Fig. 91. — Diagram illustrating the rise of arterial pressure which results from 
increased peripheral resistance. (After Lang and Manswetowa.) 



The reservoir (//) is filled with water which escapes through P 
(the capillaries) by means of A arteries). If the stopcock be wide 
open, water will rise in the standpipe M 1 pressure) to the p.oinl n. 
If the stopcock be partially closed (increased peripheral resistance) 
it will rise to m, and even with a diminished head in // (lessened 
cardiac power) it will still rise to 0. 

A rise in the pulse-pressure during symptomatic improvement is 
less constant, and when present it is more frequent in mitral lesions 
and in emphysema. This has been explained as due to the fact 
that under these circumstances the loss of compensation is the 
result of right heart weakness, the left heart being unaffected and 
being opposed by a greater peripheral tonus. With a constant 
blood flow, aortic pressure and pulse-pressure increase coincidently. 1 
The reestablisliment of compensation must be associated with 
better cardiac filling and more forcible contraction. As soon as an 
improved circulation occurs, oxygenation of the blood is increased 
and peripheral spasm relaxes. 2 Several observers have constantly 

1 Furst and Soetbeer: Untersuchungen u. d. Beziehungen zw. Fiillung u. Druck 
m. d. Aorta, Deutsch. Arch. f. klin. Med., 1907, xc, 190. Strassburger: Ueber d. 
Einfluss f. Aortenelastizitat a. d. Verhaltniss zw. Pulsdruck u. Schlagvolumen d. 
Herzens, ibid., 1907, xci, 378. 

2 Lang, G., and Manswetowa, S.: Zur Frage d. Veriinderung des arteriellen Blut- 
druckes bei Herzkrankheiten wahrend d. KompensationsstSrung, Deutsch. Arch. f. 
klin. Med., 1908, xciv, 455. (See Bibliography and numerous statements in the 
foregoing discussion.) 



248 BLOOD-PRESSURE IN CARDIAC DISEASE 

found that a temporary increase of pulse-pressure occurs at the 
beginning of compensatory reestablishment. 

In compensated mitral obstruction pressure is, owing to peripheral 
vasoconstriction, more often above than below the normal. The 
pulse-pressure is small. Hypotension may therefore be of some 
value in diagnosticating between hemoptysis due to tuberculosis 
and that due to mitral obstruction. 

Lagrange 1 found the arteriocapUlary pressure (as indicated by 
the sphygmomanometer of Bouloumie) in mitral stenosis higher 
than normal, the arterial pressure about normal. In cases asso- 
ciated with arteriosclerosis, pressure was distinctly elevated (180 
mm.), and in such cases a sudden fall was prognostically grave. 

The blood flow in two cases of mitral obstruction studied by 
Means and Newburgh 2 showed a very small (1.3, 2.2 L per minute, 
normal 4 to A\) volume, together with a high coefficient of utiliza- 
tion of the oxygen-carrying capacity and an increase in hemoglobin. 
This combination of factors would seem to act conservatively in 
these patients, since relatively more oxygen is carried to the tissues 
by a given quantity of blood flow. 

Edema and Blood-pressure. — It has been suggested that edema 
increases blood-pressure by mechanically compressing the peripheral 
arteries, and that this plays a part in the increased pressure which 
is seen in broken compensation. If it ever plays any such part it 
must be a very insignificant one, since ordinarily edema and vascular 
tension bear no constant relation to each other. Pressure may 
either rise or fall while dropsy increases or diminishes. The occur- 
rence of edema in cardiac no less than in renal disease is not, as 
formerly supposed, merely a question of hemodynamics but is 
closely related to certain metabolic abnormalities, notably the 
retention of sodium chloride in the body. 

Experimentally pvlse-pressvre bears a definite relation to edema 
and infarction. It has been shown that edema, which occurs read- 
ily in perfused organs, may be largely prevented if an intermit- 
tent — pulsating — pressure be employed. 3 Erythrocytic diapedesis 
occurs at the point at which pulsation of the arteries can no longer 
be seen. 4 

In uncomplicated valvular disease in which an increased pressure 

1 Essai de Spnygmotonometrie clinique appliqu6o aii diagnostic du retrgcissement 
mitral, Arch. g6n. de M6d., L908, excix, 293. 

2 Tr. Assn. Am. Phys., 1915, xxx, 51. 

• Hamel: Die Bedeutungdes Pulses f.d. Blutstrom, Ztschr. f. Biol., 1889, xxv, 447. 
4 Mall and Welch: Thrombosis and Embolism, Albutt's System of Medicine, 
L899, p. 254. 



i:\TRASYSTOLlc ARRHYTHMIA 249 

exists no effort should be made to lower tension l>\ means of vaso- 
dilator remedies. Vasoconstriction is in these cases an efforl to 
correct myocardial insufficiency by inciting the ventricles to restore 
the proper output (Starling). An increased pressure during com- 
pensation may be necessary to insure the requisite speed of capillar^ 
flow. 1 (Seep. 296.) 

Myocardial Disease. Much of what I have stated regarding 
arteriosclerosis and arterial hypertension applies to myocardial dis- 
ease, because the latter generally is verj frequently the terminal 
stage of the former. Since it is impossible to differentiate clinically 
between differenl forms of myocardial degeneration, they may be 
considered as a group. 

As in valvular lesions, blood-pressure in chronic myocardial dis- 
ease is variable, although with the exception of the terminal stages, 
an increase will usually be found. The pulse-pressure is often 
small. Such a finding is common even when functional capacity 
is far from good. In these eases exertion produces oppression, 
dyspnea, etc., and a fall of pressure. Stewart found a slow blood 
flow as low as 0.2 gm. per 100 c.c. per minute as compared with 
a normal of 3 to 5 to 14 gm. Not infrequently myocardial cases 
show a normal systolic but a high diastolic pressure. Rosenfeld 2 
believes that a very low blood-pressure associated with mild 
anginal attacks, dilatation of the left ventricle and aorta, and 
auricular fibrillation, especially if associated with a positive Wasser- 
mann reaction, points strongly to syphilitic myocarditis. Sal- 
varsan must be administered with caution in these cases owing 
to its tendency to lower blood-pressure and bring on tachycardia. 
The absence of hypertension and cardiac hypertrophy in syphilitic 
arterial disease was pointed out by Cautley. 3 

Extrasystolic Arrhythmia. — The genesis of this form of cardiac- 
irregularity may be closely associated with arterial tension. Both 
experimentally and clinically it is often induced by increasing 
arterial pressure and abated when tension is diminished. When 
due to such a cause it may be interpreted as an indication that the 
heart is beginning to stagger under its burden. The extrasystoles 
themselves are less forcible than the regular contractions, and the 
ventricle is less well filled. Hence their systolic pressure level is 
lower than that of the regular contraction. The postextrasystolic 



1 Korke, V. T. : Systolic Blood-pressure in Diseases of the Heart, Lancet, Decem- 
ber 2, 1911, p. 1547. 

2 TJeber Syphilitische Myocarditis, Deutsch. med. Wchnschr., 1914, xl, 1044. 
3 Lancet, April 6, 1901. 



250 BLOOD-PRESSURE IX CARDIAC DISEASE 

pressure is often higher — prolonged diastole. The existence of 
hypotension in association with extrasystoles, other things being 
equal, points to a purely functional origin of the arrhythmia. 

Tachycardia. — Low blood-pressure is generally associated with 
tachycardia, especially in fevers. When heart action is very rapid, 
diastole is too short to allow adequate venous inHow, and hence 
output must fall. In such discs the hypotension may in part be 
responsible for the rapid pulse, although both symptoms are in the 
main the result of toxemia. In paroxysmal tachycardia there is, 
during the paroxysm, often a fall of the arterial and a rise of the 
venous pressure due to insufficient diastolic filling of the ventricles. 

Bradycardia. — Bradycardia is often accompanied by relatively 
slight blood-pressure changes. With a very slow pulse, however, 
the diastolic pressure is generally considerably below the normal. 
Gibson has reported heart block associated with a pressure of 
V,," mm. In the cases of Adams-Stokes disease coming under my 
personal observation the following readings were made: 

% 30 ^ 24 ™ 48^, 36^, 30?, 30^, Pulse ""»" 



85 85 65 65 85 diastolic 

Bradycardia is sometimes due to increased arterial tension. The 
latter condition produces central stimulation of the vagus, and this 
in turn a slowing of the pulse. When the hypertension is gradual 
in onset, an increased pulse rate is the rule, but when it is sudden, 
as occurs experimentally and in cases of acute nephritis, brady- 
cardia is more apt to result (Krehl). 

Pulsus Alternans. — A marked increase in pressure is the rule; in 
fuel, this form of arrhythmia, which is generally attributed to fail- 
ure of ventricular contractility, may disappear with a fall, and 
recur with a rise, of arterial pressure. Herrick 1 finds the sphygmo- 
manometer useful not only in detecting latent cases of pulsus 
alternans, but also in increasing the tactile perception of the alter- 
nation. The cuff is inflated to the point at which the pulse rate 
becomes halved. If the cuff pressure is allowed to fall somewhat 
lower all the beats will come through, but the alternation in their 
size becomes more noticeable than when the arterial lumen is 
uncompromised. 

Auricular Fibrillation. In auricular fibrillation successive pulse 
waxes are so extremely variable in both size and tension that it 
is not possible to draw any accurate conclusions from ordinary 

i Jour. Am. Med. ksm., February 27, L915. 



AURICl L w,' FIBRILLATION 



251 



blood-pressure readings. The largest pulse waves are often 10 to 
50 mm. higher than the smallest. An approximate average pre ure 
m;i\ l>c obtained, as suggested by Janeway, by noting the pressure 

of the largest and the smallest pulse waves separately, a method 
which emphasizes the number of waves which tail to come through 
at a certain pressure. Silherberg 1 employs a Mackenzie polygraph, 

upon which he records the pulsations of both radial arteries, one of 
them under increasing degrees of cuff pressure, thus obtaining a 
graphic record of the relative pressure of different systoles (Figs. 
92, 93 and 94). 

•*■■ : 



90 



"iVrt"*' 



130 



HO 



Fig. 94 
Figs. 92, 93 and 94. — Three strips of tracing (right and left radial) taken from 
the same patient. Fig. 92, before brachial compression; all the beats come through. 
Fig. 93, the smallest beats (,rx) disappear at a pressure between 90 and 100 mm. Hg. 
Fig. 94, the largest beats fail to record at a pressure of 140 mm. Hg. 

A more satisfactory method of estimating blood-pressure in 
auricular fibrillation has been suggested, based upon what is known 
as the relative pulse deficit. 2 

The pressure in the cuff which has been raised above the highest 
systolic pressure is allowed to fall 10 mm. at a time and interrupt- 



1 British Med. Jour., April 6, 1912. 

2 James, W. B., and Hart, T. S.: Auricular Fibrillation; Clinical Observations on 
Pulse Deficit, Digitalis, and Blood-pressure, Am. Jour. Med. Sc, 1914, cxlvii, 03. 



BLOOD-PRESSURE IN CARDIAC DISEASE 



edly checked. A count is now made of the number of pulse waves 
which pass the cuff at a given pressure, in relation to the number of 
cardiac contractions as counted per minute over the precordium 



On. Xov. ><>«• 


i:j lt|lG 18 Jci Ji j:> -i; •_•> •_•!> M l :» g ;> n 1:1 16 -'1 J- -J4 ■.':> 1; 1 * 5 7 8 9 1U 11 12 U) 


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^H 


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L^H 


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II 1111 iif HI III 11 lllllH 


Bk ■ U jH BiA 


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HI i^HV ^V"~-^ H nr^HFi 


V% s ' ■kV Pf^ ^«| 




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-_j5h-,c*^i±ii- \ :r n -- \ 


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_„j _ v_ _*fif__. 


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±±::::::::::::::::::::::::::::::::±:::" !::±:::::::::::::::::::::: 


1Q DiGi- rmc ;»f. ran »f. 

T * L| s 60 0C888 400 1 i 15 15 15 15 3 3 8 880000 44 48 888 8 88 


30e f cJ UP--BEI UP BEC UP- 



FlG. 95. — The shaded area represents the pulse deficit; the upper edge is the 
apex rate: the lower edge is the radial rate. The broken line indicates the range 
of the "average systolic blood-pressure." Digitalis figures indicate minims of the 
tincture and dram- of the infusion. October 13, admitted to hospital. November 
3, up in chair half an hour; November 9, up in chair two hours. December 4, up in 
chair four hours. At this time she had a crop of external hem' rrhoids which caused 
much distress. (James and Bart.) 

by an assistant. The excess of the latter over the former consti- 
tutes the "deficit." The process is repeated until all the beats 
traverse the cuff— until there is no deficit. 



Brachial pressure. 


Radial count. 


Apex count 


1 in mm. 





64 


130 " 


50 


64 


120 " 


58 


64 


110 " 


62 


64 


100 " 


62 


64 



In this case there is no actual deficit, because below 100 mm. 
all the beats reach the periphery. But there is a relative deficit 
which occurs as soon as pressure is raised above 100 mm. 
The "average systolic pressure" is determined as follows: 
"The apex and radial are counted for one minute, then a blood- 
pressure cuff is applied to the arm, and the pressure raised until 
the radial pulse is completely obliterated; the pressure is then low- 
ered 10 nun. and held at this point for one minute while the radial 



AURICULAR ARRHYTHMIA 253 

pulse is counted; the pressure is again lowered 10 mm. and a sec I 

radial count is made; this count is repeated at intervals to LO nun. 
lowered pressure until the cuff pressure is insufficient to cul off 
any of the radial waves (between each estimation the pressure on 
the arm should be lowered to 0). From the figures thus obtained 
the average systolic blood-pressure is calculated by multiplying 
the number of radial beats by the pressures under which they 
came through, adding together these products and dividing their 
sum by the number of apex beats per minute. The resulting figure 
is what we have called the 'average systolic blood-pressure.' 
The following observation made on a patient will indicate the 
method of computation: 
B. S., April 29, 1910. Apex, 131; radial, L01; deficit, 30. 

Brachial pressure Radial count. 

100 mm. 

90 " 13 13 X '.'ii l I7n 

80 " 17 - 13 = :-!4 > 80 2720 

70 " 77, - 17 -- 28 ■ 7ii = I960 

• 60 " 82 - 75 = 7 X 60 = 420 

50 " 101 - 82 = 19 X 50 = 950 

Apex = 131 17220 

Average systolic blood-pressure 55 + 

Kilgore 1 has suggested the following method which is more 
accurate than that just described. 

The Fractional Method. — This method differs from that of James 
and Hart in the fact (1) that diastolic readings are made by deter- 
mining the fifth auscultatory phase, and (2) by a different interpre- 
tation of the systolic readings. 

These readings are made at 5 instead of 10 mm. Hg. intervals, 
and are tabulated as having an average value of 7.5 mm. Thus in 
a given case with 88 pulse beats per minute and a pressure ranging 
between 110 and 145 mm. the chart and figures shown on page 
254 were obtained. 

Lewis, 2 who experimentally investigated the effect of auricular 
fibrillation upon the circulation as a whole, found that blood- 
pressure, while it might rise or fall or remain unchanged, generally 
fell, soon to regain its original level. The volume of the intestines 
behaved in a similar manner; the venous pressure in just the oppo- 
site manner. From these experiments it appears that auricular 

1 The Fractional Method of Blood-pressure Determination, Arch. Int. Med., 1915, 
xli, 939. 

2 Fibrillation of the Auricles, its Effect upon the Circulation, Jour. Exp. Med., 
1912, xvi, 395. 



2M 



BLOOD-PRESSURE IN CARDIAC DISEASE 

MM. HG. 





















1 


^ „. 




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DIASTOLIC 


:OUNTS (ALL SOUNDS} i-fl ' 




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1"~" 




;:£ ±i - 


rr* 




-— ' — 


















- - ■ - ; ] ; - ' ; ■■•'-; H - 



10 20 30 40 50 60 70 80PERMIN. 

Fig. 96.- -Showing the relation of systolic and diastolic pressures in a typical case 
of auricular fibrillation in which the diastolic pressure of one cycle never exceeds 
the systolic pressure of another. The numbers at the left indicate millimeters of 
mercury pressure in the pneumatic cuff; those at the bottom the rate per minute of 
beats counted in various ways. The upper line here represents the results of palpa- 
tory systolic counts, the lower line fifth phase diastolic counts. 
(«) (&) (c) 1 

6 -0=6 6 X 147.5 = 

8-6=2 2 X 142.5 = 

14 - 8 = 6 6 X 137.5 = 

38 - 14 =24 24 X 132.5 = 

60 38 22 122 X 127.5 



76 'in = 16 
82 - 76 6 

ss _ 82 = 6 



16 X 122.5 = 
6 X 117.5 = 
6 X 112.5 = 



885 

285 

825 

3,180 

2,805 

1,960 

7(ir. 

675 



1 1,320 h 88 = 128.6 = average 
systolic pressure. 
■In the figures shown herewith the numbers on the base line correspond to the 
figures in column a In the above tabulation; i. e., they represent total numbers of 
waves felt or sounds heard al the corresponding cuff pressures. For some purposes 
it would l>e .-in advantage to construct curves in which the base-line figures repre- 
sented the quantities in column c, i. <■.. the number of beats which have a certain 

In such a figure taken from ;l normal ease there would be two narrow 
lount of the pulse-pressure, while if it. were from a very 
case the diastolic and systolic curves might overlap. The work of con- 
structing these additional curves is unnecessarj if it is remembered that their lateral 
extent would depend on the slope of the curves here employed. In the figures 
herewith, the more uniform the pressure of the beats, the more nearly horizontal 
the lines, and the more variable the pressure the more sloping the lines. 



I'h'ACTICAL CONSIDERATIONS 255 

fibrillation does not necessarily entail any marked change on the 
circulation as a whole. In human disease, however, we are dealing 
not only with an arrhythmia bu1 with ;i diseased myocardium as 
well, so thai marked differences are readily accounted for. 

1 )oubtless part of the blood-pressure variations which occur in as- 
sociation with various forms of arrhythmia are the result of mechan- 
ical respiratory influences. While Henderson has emphasized the 
fact that heart-rate changes in man have an important part in 
blood-pressure variations, and while in some cases they are the 
only determining influence, yet this i-, according to Wiggers, 1 not 
the only nor even the main factor in the majority of cases. 

Practical Considerations. — Blood-pressure observations are often 
distinctly useful in the diagnosis of valvular lesions. A high sys- 
tolic and a low diastolic pressure suggests aortic insufficiency, the 
murmur of which is often low-pitched and easily overlooked. If 
a double aortic murmur is heard, blood-pressure readings will often 
help us in deciding whether the obstruction or the insufficiency is 
the preponderant lesion. In aortic obstruction the pulse-pressure 
is small. Again, in case of a presystolic murmur associated with 
an aortic lesion, the sphygmomanometer may help us in deciding 
whether we are dealing with a Flint murmur or with an additional 
mitral obstruction. In the latter case the pulse-pressure is small 
and the systolic pressure relatively normal. 

In cases presenting the symptoms of angina pectoris a high 
blood-pressure is evidence in favor of an organic lesion, although 
the occurrence of a normal pressure by no means excludes it. Well- 
marked hypotension in patients complaining of weakness and vertigo 
with dyspnea on exertion, points to a loss of vasomotor tone rather 
than to a myocardial lesion in which pressures are generally normal 
or slightly increased. 

Many cardiac murmurs in advanced life are due to roughening 
and sclerosis of the valves, although their actual functional capacity 
may be but little impaired. Here, again, the absence of significant 
pressure abnormalities may help in solving the problem. Some 
light may also be thrown upon the strength of the heart muscle 
by the duration of the different auscultatory phases (see p. 72). 
A certain amount of the increased tension seen in cardiac patients 
is due to their psychic state (discomfort, anxiety, fear, etc.). Jane- 
way has suggested that a dose of morphin, which is often followed 
by marked and often lasting improvement in such cases, may 

1 Does Cardiac Rhythm alone Determine Blood-pressure Variations? Jour. Exp. 
Med., 1914, xix, 1. 



256 BLOOD-PRESSURE IN CARDIAC DISEASE 

also show how much of the increased pressure is due to the mental 
condition. 

Pericardial Effusions. — It has been known ever since the experi- 
ments of ( lohnheim that a rise of intrapericardial pressure is followed 
by a decreased aortic pressure, and vice versa. 

Experimental Data. — Under normal circumstances the peri- 
cardium — which is in health indistensible and capable of with- 
standing a pressure sufficient to rupture the myocardium — acts as 
a protective covering to the heart under conditions of strain. It 
prevents cardiac dilatation beyond a certain point and in so doing 
adds measurably to the efficiency of the tricuspid valve. 1 It pre- 
vents the further inflow of venous blood when a certain stage of 
dilatation has been reached, which, did it not occur, would lead 
to interstitial hemorrhage and myocardial rupture. 2 It has been 
shown that when the heart of a curarized animal (cat) is enclosed 
in a glass cardiometer very small changes of pressure in the cardi- 
ometer system produce comparatively wide changes in the carotid 
pressure. Thus, an increase of 1 mm. Hg. of extracardial pressure 
caused a fall of 8 mm. in the systolic pressure. These changes 
occur within the space of time occupied by two heart beats. If 
intrapericardial pressure is raised with the heart in situ essentially 
similar results are obtained 3 (see p. 44). 

Clinical Data. — In pericardial effusions we therefore find a Interred 
arli rial tension and a decreased puke-pressure. Owing to the 
increased intrapericardial pressure, less blood reaches the right 
auricle, the blood flow into which is normally abetted by the fact 
that extrathoracic pressure is higher than that in the venae cava?. 
Hence a smaller volume of blood reaches the left ventricle; and 
since the systolic output is decreased, arterial pressure must fall 
unless these effects are counter-balanced by a peripheral vasocon- 
striction. These same causes produce an increased venous pressure 
which is compensatory in nature; for if venous pressure were to 
fall below intrapericardial pressure no blood would reach the right 
auricle. Intrathoracic pressure being lower during inspiration and 
higher during expiration, it is evident that when venous and intra- 
pericardial pressures are nearly equal the act of breathing will have 
an alternately inhibiting and accelerating effect upon the blood 
How to the heart, which results in the pulsus paradoxus — decreased 
volume during inspiration. For the reasons just stated, this 

1 Barnard: Proc. Jour. Physiol., 1898, xxii, 43. 
- Kuno, ^ .: The Significance of the Pericardium, ibid., 1915, p. 1. 
3 Lewis, Th.: The Influence of [ntrapericardial Pressure upon the Inspiratory 
Rise <>f Blood-pressure in Vagotomized Cats, Jour. Physiol., March 21, 190^, xxxvii. 



BLOOD PRESSURE AS A THERAPEUTIC INDEX 257 

phenomenon only occurs at a certain stage (broken compensation), 

and in certain cases of pericardial effusion. 1 

Bronchial Asthma.— Asthmatic attacks are nearlj always accom- 
panied by hypertension. This may result from 1 * asphyxia or 
(2) complications, especially nephritis. The acl of coughing pro- 
duces a temporary marked increase of tension which is coincident 
with the expiratory movement. 

Blood-pressure as a Therapeutic Index. The Fact thai muscular 
efficiency can be increased by exercise and that this rule applies to 
the heart as to other muscles was affirmed by Oertel, who intro- 
duced graduated hill climbing as a therapeutic measure. Resisted 
exercises constitute a well-known pari of the Nauheim treatment. 
Dumb-bell exercises have been successfully used by Barringer and 
Tecschner. 2 They employ certain flexion and extension movements 
with dumb-bells and bars of a known weight, which renders an 
approximate estimation of the work done in foot-pounds possible. 
The exercises which are carried on for short intervals (30 to L20 
seconds, witli the glottis open, followed by five minutes of rest) 
are gauged by their effect upon blood-pressure and pulse rate. If 
the former falls and the latter rises, the exercise is too severe and 
must be diminished. The cases treated included chronic valvular 
disease with varying amounts of decompensation. Acute pro- 
cesses, recent embolism and very high Mood-pressure were con- 
sidered as contra-indications. Many of the cases showed a marked 
increase in efficiency associated with subjective improvement. 
As a rule the aortic cases (in young adults) improved more rapidly 
than those with mitral disease. 

The benefits of exercise in cardiac disease are to be attributed 
to (1) improved coronary circulation; (2) increased peripheral 
blood flow; (3) assistance to the venous and (4) lymphatic, circu- 
lation; (5) enlarged lung capacity and (6) their encouraging psychic 
effect. 

'Calvert, W. J.: Pulsus Paradoxus in Pericarditis with Effusion, Jour. Am. 
Med. Assn., 1907, xlviii, 1168. 

2 The Treatment of Cardiac Insufficiency by a New Method of Exercise with 
Dumb-bells and Bars, Arch. Int. Med., 1915, xvi, 795. 



17 



CHAPTER XI. 

BLOOD-PRESSURE IN ARTERIOSCLEROSIS— VASCULAR 

('RISKS. 

About one-third <>f nil cases of well-marked peripheral arterio- 
sclerosis have normal or subnormal pressures. In the remaining 
two-thirds the pressure is variably increased, depending mainly 
upon the degree of renal involvement. Arteriosclerosis is selective 
in it-- location; thus syphilis attacks the ascending aorta. Individ- 
uals who perform severe physical labor often develop peripheral 
vascular lesions of extreme degree, yet the pipe-stem radial artery 
is often a relatively benign type of the disease. Savill's 1 investi- 
gations based on 400 autopsies on individuals of and over sixty 
years of age, showed that extensive patchy atheroma is consistent 
with extreme longevity, with an entire absence of symptoms or 
of vascular complications. This same statement is applicable to 
marked generalized intimal and adventitial sclerosis so long as the 
medial arterial wall is relatively uninvolved. The foregoing state- 
ments are borne out by Ophiils's studies, 2 who failed to find cardiac 
hypertrophy in 35 per cent, of all cases of marked arteriosclerosis. 

The hypothesis advanced by Hasenfeld and Hirsh that arterio- 
sclerosis is unaccompanied by increased blood-pressure unless the 
arterioles in the subdiaphragmatic and splanchnic domain are the 
seal of disease has caused much discussion and is now not generally 
accepted. Sclerosis of either the large or the small splanchnic 
vessels is not a common finding. A spastic condition of these 
vessels may exist, however, which will increase tension, although 
this is not apt to occur once the vessels are definitely sclerotic. 

Longcope and McClintock 8 found that compression of the 
superior mesenteric artery and the celiac axis gives rise constantly 
to an elevation of blood-pressure which may last for at least an 
hour. This rise of pressure is mechanical, due not to a reflex action 
but to an increased amount of blood in the general circulation. 
The pressure remains increased until the excess of blood accumu- 

i Lancet, L904, p. 506. 

•Subacute and Chronic Nephritis as Found in One Thousand Unselected Autop- 
sies, Arch. Int. Med., L912, ix, 158. 

• The Effect of Diminished Blood Supply t<> tin' Intestines upon the General 
Circulation, Johns Hopkins Med. Bull., 1910, xxi, No. 234. 



BLOOD-PRESSURE l\ IRTERIOSCLEROSIS 259 

lates in the ramifications of the splanchnic vessels by way of col- 
lateral anastomosis. But even if this constriction is maintained for 
several months in dogs neither hypertension nor cardiac hyper- 
trophy develop. 1 This may be due to the compensatory effed of 
an efficient collateral circulation. Furthermore, Marchand 2 was 
unable to establish any definite relationship between cardiac hyper- 
trophy and the degree of arteriosclerosis of the abdominal aorta or 
the splanchnic vessels. 

The evidence now at hand points strongly to the view that 
hypertension when present in arteriosclerosis is due to spasm or 
sclerosis of the systemic arterioles. While, therefore, the dictum that 
a man is as old as his arteries still holds good, yet it appears thai 

the c lition of the smallest arteries is more importanl than the 

largest ones; and, further, we are not justified in assuming that 
because the radial artery shows extensive disease, the more vital 
arteries and arterioles are therefore correspondingly involved. 

Thoma's injection experiments upon the cadaver showed that 
fluid could be injected into arteriosclerotic much less rapidly than 
into non-sclerotic subjects and, further, that a much -mailer quantity 
of fluid sufficed in the former instance to produce edema, [n other 
words, although the vascular lumen is not much reduced in size 
the permeability of the capillaries is diminished and in all probability 
their area diminished while the resistance in the arterioles is 
increased. 3 

The causes and pathology of vascular disease cannot be dis- 
cussed here, and only the phases of the problem which have ;i 
distinct bearing on blood-pressure will be considered. 

Osier states that (1) high blood-pressure is one of the causes of 
arteriosclerosis — the others being (2) wear and tear, (3) infections 
and (4) intoxications. The following classification of arteriosclerosis 
has been suggested by Allbutt: (1) Toxic: plumbism, diabetes, 
infectious diseases, notably syphilis; (2) involutional^', from senile 
degeneration; (3) secondary following hypertension. 

Clinically, such changes are manifested by arterial hypertension, 
cardiac hypertrophy, albuminuria, and varying subjective phe- 
nomena; the first of these resulting from tonic contraction of the 
arterioles and capillaries. With prolonged increase of pressure the 
systemic arteries at first become thickened and hypertrophied. The 
cerebral vessels and the aorta being less liberally endowed with 

1 The Effect of Permanent Constriction of the Splanchnic Arteries and the Asso- 
ciation of Cardiac Hypertrophy with Arteriosclerosis, Arch. Int. Med., 1910, vi, 439. 

2 Verhandl. Kong. f. inn. Med., 1904, xxi, 60. 

* Mott, F. W.: Albutt's System Med., vi, 327. 



260 BLOOD-PRESSURE IX ARTERIOSCLEROSIS 

muscular tissue dilate, and, either with or without aneurysmal 
change, not infrequently rupture. The vascular damage in these 
rases is largely mechanical, as in occupations associated with hard 
labor, whereas arterial degeneration in the organs, especially the 
kidneys, results mainly from toxic irritation. As a rule arterio- 
sclerosis is unassociated with arterial hypertension. The blood- 
pressure in arteriosclerosis is of course higher than in youth, but 
the degree and the constancy of the elevation depend chiefly upon 
the location and character of the arterial changes, especially upon 
the extent to which the peripheral arterioles are affected. Exten- 
sive, spontaneous and often uncxplainable variations of pressure 
are of frequent occurrence. 

Blood-pressure in Old Age.— In 1.10 cases ranging in age between 
sixty-five and ninety-five years, Bowes 1 corroborated the earlier 
studies of Wildt 2 to the effect that during very advanced years a 
pressure previously high tends to recede. This is shown in the 
following tables: 

The Average Blood pressure of Both Men and Women. 

Number Systolic Diastolic Pulse- 

examined, pressure. pressure. pressure. 

65 to 00 years 32 151 82 65 

70 to 74 " 39 160 86 73 

75 to 79 " 38 166 so 79 

80 to 84 " 27 175 84 83 

85 to 89 " 7 170 90 77 

90 to 94 " 7 142 81 01 

Tin-; Average Blood pressure of the Women. 

Number Systolic Diastolic Pulse- 

examined, pressure. pressure. pressure. 

65 to 69 years 21 15 1 83 71 

70 to 74 " 20 L58 83 72 

75 1<» 70 " 24 170 ss si 

80 to 84 " 16 is:; 85 91 

85 to so " 7 170 00 77 

OKI., 01 " 3 137 80 53 

Tm; Average Blood pressure of the Men. 

Number Systolic Diastolic Pulse- 

ezamined. pressure. pressure. pressure. 

65 to 00 years 11 1 15 81 63 

70 to 74 " 10 10C, 1 75 

75 to 70 " 11 150 SO 77 

so i,, s| " 11 103 84 so 

85 t.. so " 

00 to 01 " 4 145 81 05 

Bl 1 pressure in the Aged, .lour. Lab. and Clin. Mod., 1017, ii, No. 4. 

•Ueber Blutdruck im Greisenalter, Zentralbl. f. Her/., u. Gefasskrankh., 1912, 

iv, S. li 19, 



VASCULAR REACTIONS Ih YRTERIOSCLEROSIS 26] 

Bilateral inequality of pressure is frequent in arteriosclerosi , 
and accuracy can only be obtained by repeated readings, inasmucb 
as temporary variations arc common. Large pulse-pressures are 
the rule, because the diastolic pressure remains disproportionately 
low compared to the diastolic level seen in cardiovascular hyper- 
tension. 

Arteriosclerosis per se does not necessarily cnusc hypertension. 
The actual height of the pressure depends upon I 1 the stage al 
which the pressure is observed; (2) the degree of arteriolar involve- 
ment; (3) the myocardial integrity. Some cases with pipe-stem 
arteries show relatively normal pressures, while other cases with 
fairly soft vessels show very high tension. Very high pn 
may exist without symptoms, but slight vertigo, morning head- 
ache, numbness, tingling and cramps in the legs arc to be expected. 
All of Bowes' cases which suffered cerebral hemorrhage showed 
high systolic, diastolic and pulse-pressures. 

Vascular Reactions in Arteriosclerosis. The circulation in 
arteriosclerosis differs in many ways from that in health. The 
normal arm, according to (). Midler's plethysmography studies, 
contains about 7 per cent, of blood; in arteriosclerosis this amount 
is much decreased. Abnormal local variations in blood-pressure, 
either unilateral or bilateral, in corresponding or different regions 
of the body are not uncommon in arteriosclerosis. 

In the case of normal arteries the tall of pressure in passing from 
the aorta to the periphery is gradual. The first important fall 
occurs in the capillaries. In sclerotic vessels, however, vascular 
contraction of the arterioles and small arteries i> capable of pro- 
ducing well-demonstrable pressure differences in homologous per- 
ipheral arteries. Findlay 1 found that as the age of the subject 
increased there was a constantly increasing tendency for marked 
pressure variations to occur between the central and peripheral 
arteries, e. g., brachial and digital. In the majority (80 per cent.) 
of the cases the proximal vessel showed the higher pressure. These 
findings were especially noticeable in cases of arterial hypertension 
and are apparently due to arterial contraction. 

This fact has been emphasized by Teissier, 2 who believes that 
these localized inequalities of pressure indicate the site of the arterio- 

1 The Systolic Pressure at Different Points of the Circulation in the Child and the 
Adult, Quart. Jour. Med., 1910, iv, 489. See also Pesci: Riforma Medica, June 
7, 1909. 

2 Role des Hypertensions partielles dans les determinations symptomatiques de 
l'arteriosclerose, Bull. d. l'Acad. de Med., February 25, 1908, lxxii. 



262 BLOOD-PRESSURE IX ARTERIOSCLEROSIS 

scl rotic process. Thus, if the splanchnic vessels are chiefly affected, 
hypertension is said to occur in the dorsalis pedis artery, while 
increased tension in the temporal or the radial arteries points 
respectively to involvement of the intracranial or the intrathoracic 
Is. This he explains as due to a segmental phenomenon to 
which the peripheral and the deep-seated arteries react similarly. 
1,, on e case increased pressure in the temporal artery was soon 
followed by the appearance of glaucoma on the same side. In 
another case a similar pressure increase preceded attacks of facial 
paralysis, vertigo, and apoplectiform manifestations. 

These observations are of great interest but must be accepted 
with considerable reserve on account of the possibility of instru- 
mental error. The normal pressures as obtained with the Potain 
apparatus, which Teissier used, are 16 to 18 cm. in the radial; 13 
to L5 in the dorsalis pedis; and 8 to 12 cm. in the temporal arteries. 
Even if careful allowances are made for postural variations, the 
unavoidable margin of error would often be greater than the actual 
supposedly abnormal pressure variations. (See also under Func- 
tional Tests.) 

Inequality of the pressure of the pulse on the two sides of the 
body (5 to 15 mm.), if constantly present and not attributable to 
any local abnormality, often points to arteriosclerotic changes. 
Engel 1 believes that this sign may be useful in diagnosticating 
between primary nephritis and arteriosclerosis. (See Aortic 
Aneurysm.) 

Recent observations of Pierret made with the Pachon apparatus 
on the pressures of the radial and tibial arteries have shown in 17 
out of 20 cases higher readings in the lower limb (30 mm. systolic, 
in mm. diastolic). Heitz- found that the arm and leg readings 
differ very considerably, depending on the size of the cuff employed 
and whether the Pachon or the Riva-Rocci instruments are used. 
The rapidity of transmission of the pulse wave depends upon both 
the condition of the vascular wall, and to a less extent upon the 
beighl of blood-pressure. The normal rate is 8.3 to 12 m. per second. 
I,, arteriosclerosis the rate has been found increased to 10.1 m. 
(Friberger 8 ), 23 m. (Miinzer). 4 In dicrotic pulses the transmission 

Berl. i lin. Wchnschr., September 20, L909, xlvi. 

I,, Mensurations de Pression dans lea uteres des Membres Enferieures, Aremv. 
dee maladies du coeur des Vaisseaux e1 du Sang, April, 1913, p. 285. 

eUengeschwindigkeit bei Arterien m. fuhlbarer Wandverdickung, Deutseh. 
Arch. f. klm. Med., 1912, evii, 280. , 

• Die Fortpflanzungsgeschwindigkeil der PulsweUen in Gesunden ... krankhafl 
veranderten Blutgefassen, Kong. inn. Med., 1912, xmk, 131. 



VASCULAR REACTIONS l\ ARTERIOSCLEROSIS 263 

is delayed. This rapid transmission of the pulse wave, a sociated 
with a relatively low diastolic pressure often leads one to over- 
estimate the \ igor of the pulse. The rapiditj of pulse transmi ion 
in different valvular defects depends far more upon the degree of 
tension and of arteriosclerosis than upon the character of the 
lesion. 1 (Sec Aortic Insufficiency, p. 242.) 

The Nitrite Test. Rzentkowski 2 found in healthy subjectsonly 
a slight and brief diastolic fall after the inhalation of amy] nitrite. 
In arteriosclerosis, on the other hand, much greater and more pro- 
longed lowering occurred despite increased cardiac activity, Me 
interprets these facts as indicating that the splanchnic vessels have 
lost their compensatory contractility, which in normal individuals 
prevents much disturbance of tension. Arteriosclerotic hyper- 
tension may therefore (since the peripheral vessels still retain their 
power of dilating) be regarded as due to prolonged contraction of the 
arterioles. Whether this explanation be corred or not the practi- 
cal procedure may he of some value a- a tesl of arterial functiona- 
tion. F. Franck states that permanent hypertension cannot he 
due to vasoconstriction, a muscular spasm which he believes can- 
not persist indefinitely, lie calls attention to the fact that vaso- 
constriction in one locality is sooner or later always counterbal- 
anced by vasodilatation elsewhere. 

The Stasis Reaction.— The blood-pressure is taken in the recum- 
bent posture by the auscultatory method. Following tin-, the 
circulation in three extremities is occluded by inflation of rubber 
cuffs. This procedure in normal individuals when maintained for 
five minutes usually produces a rise of pressure of from 5 to 10 
mm. Hg. In arteriosclerotics the usual average reaction is 27 nun., 
the maximum 60. An increase of pressure under these circum- 
stances therefore points to arteriosclerosis. Its absence does not 
exclude this condition (Hertzell). 3 

The Ice Reaction. — Romberg and his pupils have shown that the 
application of ice to the arm normally produces a diminished local 
blood flow. In arteriosclerosis this reflex tends to be abolished. 
A merely hypertrophic artery may, however, show a normal or 
even an increased response. (See under Function Tests, p. 180.) 

1 Beitrag z. Lehre V. d. Fortpflanzungsgeschwindigkeit d. Pulswellen b. gesunden 
u. kranken Individuen, Samml. wiss. Arb. 1, Langensalze, Wendt and Klauwell, 
1912, p. 39. 

2 Untersuchungen u. d. Wirkung des Amylum nitrosum auf d. gesunde u. sklero- 
tische Arteriensy stern, Ztschr. f. klin. Med., 1909, xlviii, 111. 

3 Die Stauungsreaktion bei Arteviosclerose, Berliner klin. Wchnschr., 1913, 1, S. 
535-53S. 



264 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

The Arteriocapillary Pressure Index. — Fink' maintains that there 
is a definite and characteristic relationship between arterial and 
capillary pressure in arteriosclerosis. If an index is established 
thus: 

arterial pressure 17-18 cm. Hg. (Potain) 



capillary pressure 9-10 cm. (Gartner) 



1.80 



the quotient will lie normally between 1.5 and 2. According to 
l'ink we obtain in arteriosclerosis an index below 1.5, sometimes 
below 1. The smaller the quotient the more marked the evidences 
of circulatory insufficiency — dyspnea, edema, etc. But he specific- 
ally asserts that this is an index of circulatory efficiency and not 
one of anatomical integrity. These observations would have more 
value if the factor of instrumental error could be reduced. 

In normal individuals the local application of heat to the hand 
produces a fall of the brachial and a rise of the digital pressures. 
In arteriosclerotics negative or atypical reactions are generally 
observed (Dobrymin). 

VASCULAR CRISES. 

The term vascular crises was coined by Collier. The subject has 
been elaborately studied by Pal 2 and others, who class under this 
heading conditions which result from local or general (1) vaso- 
contraction, (2) vasodilatation, which arise without demonstrable 
anatomical lesions, the symptoms thus produced disappearing when 
normal vascular relations are reestablished. 

It is a self-evident fact that vasomotor stability, control, and 
compensation are among the most fundamental attributes of the 
animal economy. Furthermore, these intervascular relations must 
be adjusted and balanced to an extreme point of sensitiveness and 
delicacy. It is not surprising when one considers these facts, that 
vasomotor incoordination should occur, especially under certain 
conditions which appear to predispose to it. 

It has been clearly established that certain vascular domains 
are controlled by definite vasomotor centres, as the mesenteric 
vessels by the splanchnic nerves. It furthermore appears likely 
thai the enervation of such a system may be disturbed in part 
after the manner of segmental distribution, and also that the dis- 
turbances may be limited to the vasomotor element alone. There 

1 Nouvellee recherches sur la valeur, du rapport des tensions arterielles ei capillaires 
dans I'arteriosclerose, Rev. de Med., August, 1908, p. 747. 
- Gef&sskrisen, Leipsie, 1905. 



VASCl i. IR CRISES 265 

exists also a definite reciprocal relationship between certain vascular 
arras, by virtue of which a contraction in one produces a dilatation 
of the other. This phenomenon lias been ascribed l»\ some to active 
vasodilatation, by others to a purely mechanical displacement of 
blood. 

A vascular crisis may be brought about by an abnormal i l I 

contraction, or (2) dilatation, in a given vascular domain, which 
results in a certain train of direct or indirect symptoms which ma;, 
manifest themselves in the immediate neighborhood or at a distance 
from the seat of the vascular abnormality, or in general vascular 
phenomena. Certain conditions appear to predispose to such vas- 
cular crises, notably arteriosclerosis, nephritis, pregnancy, lain*, and 
plumbism. The actual symptoms produced will depend upon l 
the vascular domain involved; (2) whether vascular spasm or dila- 
tation exists; (3) whether these changes are compensated for in 
other vascular domains; I to what extent the function of the 
part or organ is affected, etc. The existence of local vascular 
crises has been indubitably demonstrated in spasmodic contraction 
of the central retinal artery (see p. 433). 

I. Crises due to Vasoconstriction. — («) The pectoral type, (6) 
the abdominal type, (c) the cerebral form, (d) the crises of the 
extremities (peripheral form), (c) the general vascular type, (/) 
paroxysmal dyspnea. 

The exact cause and mechanism of these vascular abnormalities 
is not easy to determine. It cannot be sought primarily in the 
anatomical abnormalities of the arteries in question, because the 
spastic phenomena are often manifested in vascular areas which 
are not essentially diseased or primarily affected. It may be (1) 
that stimuli which arise in the diseased area exert their influence 
upon other domains; (2) that the sympathetic system is called into 
play by local abnormalities in the vaso vasorum; or (3) that some 
pressor substance gains entrance into the blood stream. 

Angina Pectoris — Although there is still much doubt regarding 
the genesis of angina pectoris, there can be no uncertainty that 
many if not all cases are closely allied to vascular spasm. Whether 
such a contraction is purely local — limited to the coronary arteries 
— thus causing ischemia of the myocardium, or whether it be of a 
more general nature, cannot be definitely stated. Angina pectoris 
is sometimes associated with Raynaud's disease and intermittent 
claudicatio n, both of which are typical examples of local vascular 
spasm. The writer was on one occasion taking a blood-pressure 
reading during which an attack of angina occurred. The systolic 



266 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

pressure, previously 160 mm. Hg., suddenly rose to 210 mm. and 
remained at that point for the few minutes during which the pain 

lasted. In many eases of angina, however, the pressure during 
attacks is either normal or actually lowered. The latter occurs 
especially in the syphilitic cases and is what one should expect if 
coronary arterial spasm is accepted as the cause of the attacks. It 
is also to be remembered that both pain and anguish have potent 
pressor actions and that a rise of pressure when present may be the 
result and not the cause of the paroxysm. 

Anginal attacks may he preceded by or associated with evidences 
of local peripheral vascular crises — pallor, coldness, cyanosis. "It 
i- probable that by disease of the aorta its sensitive endowments, 
those which regulate blood-pressure, are disordered — exalted or 
impaired; and, during or near the attack, pain, dread or distress 
make all measurements of blood-pressures untrustworthy." 1 Tran- 
sient aphasia, paralysis, dead fingers, etc., which are also angio- 
spastic phenomena, may also occur coincidently with the par- 
oxysms. 2 Furthermore, angina pectoris and abdominalis may be 
alternately present in the same patient, and the symptoms of the 
latter are closely analogous to the abdominal vascular crises of 
plumbism, locomotor ataxia, angioneurotic edema, and purpura. 
Curschmann 3 has reported cases illustrating the development of 
angina pectoris upon a basis of or as an accompaniment to peripheral 
vasomotor cramps, emphasizing the fact that the heart is embryo- 
logically only a specialized artery, so that its connection with the 
arteries is both anatomical and nervous. 

The subjects of angina pectoris are the subjects of arterial dis- 
ease — aortic, coronary, or general — and sclerotic arteries readily 
exhibit spastic manifestations. Most of these patients have previ- 
ously had arterial hypertension for variable periods. During the 
paroxysms the pressure suddenly, markedly, and rapidly increases. 
While the rise may be abetted by the pain it is certainly not pri- 
marily caused by it, and it is often relieved by amyl nitrite. "In 
many eases the attack begins directly as a peripheral vasocon- 
strictor storm, with cold hands and cold feet, pallor of the face, 
and sweating. Nor is this simply in the so-called functional type, 
but in the severest forms an emotional disturbance may initiate a 
widespread contraction of the arteries. During the paroxysm it 



1 Albutt, C: Diseases <<( the Arteries Including Angina Pectoris, London, 191"), 
ii. 338. 
-' I >sler, sir William: Angina Pectoris, Lancet, March 12 and 26, and April 9, 1910. 
'Deutsch. med. Wchnschr., 1906, xxxii, 38. 



I ASCI l. \l< CRISES 

is by nu means uncommon to find the radial pulse od one side much 
smaller than on the other" (( )sler . 

Many but not all cases of angina pectoris show marked hyper- 
tension (190 to 220 i .)• The presence of increa ed pres ure i 

often the best indication of an organic lesion, bu1 its absence i L50 
to L60 mm.) cannol be accepted as evidence of a mere functional 
or digestive disturbance. The following table shows the blood- 
pressure findings in eases of angina pectoris seen by the writer in 
private and consultation practice: 



:le. 



No. 


Age. 


Blood 




i lutcome. 


1 . 


. 72 


L85 and 75 


1 >ea1 h in paroxysm. 


2 . 


. 73 


21 II i 


" 115 


1 )eath in paroxysm. 


3 . 


. . 49 


l in 


•• L00 


1 >eath from rupture of \ enl 


I 


60 


160 


" lin 


Unknown. 


5 . 


66 


200 


- L30 


Unknown. 


6 . 


. . 68 


138 


- 120 


1 iikiinw n. 


7 . 


. . 12 


21 1| i 


•• no 


Unknown. 


s . 


58 


200 


•• 165 


1 )eath in paroxysm. 


9 . 


. . 59 


190 


■■ L00 


Unknown. 


in . 


53 


150 


•• loo 


Living, free from symptoms 


11 


. . 7(1 


L95 


•■ loo 


Death in pai 


12 . 


. . lis 


195 


•• 85 


Death in paroxysm. 


13 . 


. . iV2 


225 


- 170 


1 leal li from apoplexy. 


11 . 


72 


160 


" 


Death sudden, third attack. 



Angina Abdominalis — the abdominal counterparl of angina 
pectoris— is more or less closely associated with the clinical picture 
of abdominal arteriosclerosis. It is based upon the presence of 
periarteritis, local thrombosis, or vascular spasm of the mesenteric 
artery, and has been regarded as an intermittent dysperistalsis 
(Schnitzler, Ortner). The clinical manifestations consisl of local 
abdominal pain, tenderness, tympanites, and of hypertension. 
Spasm of the iliac or femoral arteries leads to intermittent claudi- 
cation. Disproportionately increased femoral blood-pressure has 
been described by French authors in association with acute 
abdominal aortitis. 

Paroxysmal epigastric pain in arteriosclerotic subjects is riot 
uncommon and frequently results from organic changes in the 
gastro-intestinal tract. These attacks are sometimes brought on 
by overexertion, overeating, emotional disturbances, or by lying 
down. 

Buch 1 distinguishes two classes of arteriosclerotic abdominal 
pain: (a) abdominal cramp; (b) angina abdominalis. The clinical 
manifestations of the former, tympanites, constipation and pain, 

1 St. Petersburger med. Wchnschr., 1904, xxix, No. 27; Arch. f. Verdauungskrankh., 
1904, x, 6. 



268 BLOOD-PRESSURE /A r ARTERIOSCLEROSIS 

are associated with autopsy findings indicative of intestinal paresis, 
due to ischemia. In angina abdominalis the pain may begin in 
the epigastrium and remain localized there. 

The abdominal crises of angioneurotic edema and purpura, a 
Dumber of which have been attacked by the surgeons as a result 
of a mistaken diagnosis, have shown only local visceral edema or 
hemorrhage. 

Paroxysmal dilatation of the abdominal aorta is a condition which 
occurs chiefly in run-down, emaciated, neurasthenic women with 
ptosis of some or all of the abdominal organs. The condition is 
characterized by an abrupt forcible pulsation of the abdominal 
aorta, which is objectively visible and of which the patient is sub- 
jectively conscious. Associated with this there may be vomiting, 
epigastric pain, and sometimes faintness. The condition may 
slightly simulate aneurysm. The attacks end as suddenly as they 
begin, the termination being associated with the disappearance of 
pain and empty feelings in the epigastrium. They may last hours 
or days and during the attack blood-pressure generally is elevated 
30 or 40 mm. Between paroxysms pressure is normal. 1 

Tympanites — The subjects of cardiovascular disease complain 
greatly of tympanites. Not only is flatulence a frequent symptom 
among them, but very slight degrees of distention cause a dispro- 
portionately great amount of discomfort. How often the subject 
of angina pectoris complains only of his "stomach." 

The subject is complex. Undoubtedly vagus effects are account- 
able for both conditions, but it is further clear that abdominal 
distention mechanically interferes with heart action. Further, 
Stadler and Ilirsch 2 showed experimentally that inflation of the 
bowel from the rectum causes a marked rise in blood-pressure. 
This may be due to a hindrance of the abdominal venous circula- 
tion, but more probably results from dyspnea, as it occurs confi- 
dently with the rise of the diaphragm and fails to appear if the 
animals are enrarized or if artificial respiration is practised. 
Funder's investigations indicate that reflex rather than purely 
mechanical causes are responsible for the symptoms (see p. 43). 
Burton-Opitz has shown that distention of the intestine alone 
may cause a great diminution of the blood flow in the mesenteric 
vessels 11 (see pp. 102 and 318). 



Schleanger: Deutsch. med. Wchnschr., August 22, 1912, \ T <>. 34, p. 1592. 
' Meteorismuse u. Kreislauf: Mitt. u. d. Grenz. d. Med. u. Chir., xv, -'5 and l. 
:i Burton-Opitz, K.: Qeber d. StrSmung <lcs Blutes in dem Gebiete d. Pfortader, 
Anli. f. d. ^<^. Physiol., 1908, cxiv, 17!t. 



VASCl I \i; CRISES 269 

Renal and Biliary Colic- Attacks of renal and biliary colic may 
be associated with marked increase in arterial pre sure, a phe- 
nomenon which, while partly <lne to pain, is probablj the result of 
reflex vasomotor constriction. This sudden increase of ten ion 
may account for the production of cardiac murmurs which have 
been reported as occasionally coincident with such attacks. 1 

Cerebral Vascular Crises. The nervous phenomena of hyperten- 
sion include headache, vertigo, convuhivt seizures, paralyses (mono- 
plegia, hemiplegia), aphasia, dementia, etc. These symptoms may 
occur spontaneously and after lasting for a few hours disappear 
almost as suddenly as they appeared. The generally accepted belief 
at present is that they are due, as was first suggested by George 
Peabody, 2 to local vascular spasm. Organic lesions, hemorrhages 
or edema may perhaps also produce only transient effects, bu1 the 
duration in such cases is longer and the recover) more gradual. 
Intermittent closing and opening of the cerebral vessels is by far 
the must tenable hypothesis upon which to explain brief, tem- 
porary attacks of paralysis. Sir William Osier, 3 who has reported 
two very dramatic cases, states thai temporary aphasia is one of 
the commonest of these transient manifestations. "Inability to 
talk, the consciousness of it, no paralysis, emotional disturbance 
and, within a few hours, complete recovery," are characteristic. 
As high as twenty such attacks may occur before the patient suc- 
cumbs to some of the eventualities of arteriosclerosis. With the 
disappearance of symptoms the pressure falls 'often 30 to 50 mm.) 
to the patient's normal level. 

Vertigo is, according to Finkelnberg's 4 investigations, generally 
associated with an increase of the minimum pressure and a decrease 
of the blood-pressure quotient. This diminution of pulse volume 
which is often associated with pallor, weakness, and syncope 
apparently results from cerebral anemia. Vertigo may occur in 
either high- or low-tension cases as a result of cerebral anemia. It 
has been suggested that rotary vertigo of labyrinthine origin always 
results from bilaterally unequal vasomotor influences along some 
portion of the coordinating tracts. 5 

1 Riesman, D.: Cardiac Murmurs during Attacks of Biliary Colic, Am. Jour. 
Med. Sc, November, 1911. 

2 Tr. Assn. Am. Phys., 1891, vi, 170. 

3 Transient Attacks of Aphasia and Paralysis in States of High Blood-pressure 
and Arteriosclerosis, Canadian Med. Assn. Jour., October, 1911. 

4 TJeber Blutdruckmessung bei Schwindel, Miinchen. med. Wchnsehr.,1906, Hi, 238. 

5 Fowler, E. P.: The Origin of Labyrinthine Rest-tone, Jour. Am. Med. Assn., 
1915, lxiv, 118. 



270 BLOOD PRESSURE IN ARTERIOSCLEROSIS 

Apoplexy. Vascular rupture is naturally more apt to occur if 
blood-pressure changes in addition to being great are sudden. 
The marked pressure effects of violent muscular action, especially 
when associated with volitional effort or psychic stimulation have 
been alluded to. It i> not surprising, therefore, to find that fits 
of anger, fright, sudden stooping or heavy lifting, especially after 
a full meal, straining at stool, coitus, etc., are often the precipi- 
tating causes of vascular rupture and anginal attacks. The history 
of a preceding transient hemiplegic attack is not infrequently 
obtained in cases that ultimately succumb to apoplexy (see 
I [emiplegia i. 

Peripheral Vascular Crises — This group includes intermittent 
claudication, erythromelalgia, and Raynaud's disease. In each case 
there is believed to be a disturbed balance between the vasodilator 
and the vasoconstrictor nerves. 

There is reason for believing that some of these cases owe their 
origin to an undue excitability or exhaustion of the sympathetic 
nervous system. In a case reported by Zweig 1 there were acute 
hallucinations, recurring urticaria, and sudden symptoms of hyper- 
thyroidism. These symptoms bore no direct relation to each other 
but were all, it seemed, different expressions of sympathetic lability, 
due perhaps to some abnormality of the internal secretions, thus 
differing from the true exophthalmic goitre cases in which the 
thyroid syndrome is primary. The results of studies in this class 
of cases reported by different investigators have been quite vari- 
able. Curschmann 2 found that psychic and thermic stimuli failed 
to produce plethysmography reactions. Stewart 3 found that the 
application of cold was followed by an increased instead of a dimin- 
ished flow; and Simons' has reported great variability and asym- 
metry of vascular response. In Raynaud's <lixco.se it is believed 
that the arterioles arc so contracted that blood flow is practically 
occluded. Experimental evidence proves that this is quite pos- 
sible. Macwilliam and Kesson 6 have shown that an occlusive 
spasm capable of resisting a pressure of 440 mm. Ilg. may occur in 
diseased arteries as large as the metacarpal and metatarsal of the 

] Zur Kasuistik a. Aetiologie vasomotorischtrophischer Stdrungen, Berl. klin, 
Wchnschr., L912, riix, 2268. 

I atei uchungen ueber d. funktionelle Wrhalu>n d. Gefiissi- boi tropischen u. 
vasomotorischen Neurosen, Mtlnchen. med. Wchnschr., 1907, liv, 2519. 
Measurement of Blood Flow in the Hands, Heart, 1911, iii, 33. 
* Plethysphygmographische Untersuchungeo d. Gefassreflexe bei Nervenkranken, 

Arch. f. Anat. u. Physiol. Phys., Abteil. L910, Supplement, Band i xxix. 

Heart, 1913, iv, -".ts. 



VASCi LAR CRISES 271 

horse. Balaauw 1 has commented on the fad thai spasm of the 
retinal vessels in cases of Raynaud's disease has probablj never 
been authentically reported. 

II. Angioneurotic Manifestations. Abnormal vascularres] < 

to stimuli produce a number of differenl symptoms which have 

been designated by Cohen as vas tor ataxia. To this group 

belong dermographism, urticaria, angioneurotic edema, chilblains, 
etc. A patient studied by Hewlett 2 who had dermographism and 

chilblains reacted to the local application of lerate cold (which 

precipitated his symptoms) by a definitely increased blood How in 
the arm exposed in comparison to its fellow. The normal reaction 
to cold is of course just the reverse of this. The exudation may be 
serous or sanguineous, but in either case a marked local vasomotor 
disturbance exists. Osier has suggested thai this group of ailments 
are all due to differenl degrees of the same poison. 

Abnormal local vasomotor phenomena are also exemplified by 
(1) the tdche cerebrale a red line with white margins, produced by 
irritating the skin by drawing the finger-nail across it. This is -ecu 
in meningitis, typhoid fever, etc. (2) The white line of minimi 
insufficiency; a localized blanching of the abdominal skin pro- 
duced by means of the finger-nail, -ecu in Addison's disease and 
other conditions associated with low blood-pressure. It is directly 
due to local reflex capillary spasm. Neither of these two conditions 
is constant, nor diagnostically of much importance. 

Vascular Crises in Children. — While vascular crises are chiefly seen 
in arteriosclerotic individuals, angiospastic manifestations have 
also been described in children. Thus Kirsclr has reported attacks 
of localized gastric pain, associated with a heaving cardiac impulse, 
tortuous carotids, and a tense and pulsating abdominal aorta, 
which he attributes to vascular spasm. Hamburger also calls atten- 
tion to certain subjective symptoms relating to the heart, and to 
objective vascular manifestations due to this cause. 4 

Under the former are found palpitation, unpleasant sensations 
in the precordium, such as a "stitch," and a feeling of oppression. 
Palpitation occurs after physical exertion and to a less degree after 
psychical disturbances. In marked cases more or less pain and 
dyspnea may occur, and even symptoms comparable to the angina 
pectoris of adult life. These symptoms are, however, rare in com- 

1 Die Augen-syinptome d. Raynaudschen Krankheit, Augenheilk., 1913, ix, Heft 5. 

2 Active Hyperemia following Local Exposure to Cold, Arch. Int. Med., 1913, 
xi, 507. 

3 Gefasskrisen im Kindesalter: Mitteil. d. Gesellsch. f. inn. Med. u. Kinderheilk. 
Wien, 1912, ii, S. 190-194. 

4 Miinchen. med. Wchnschr., 1911, lviii, 2201. 



272 BLOOD-PRESSURE IN ARTERIOSCLEROSIS 

parison to palpitation. Objectively there is found a heaving some- 
what diffused apex beat, and slight epigastric pulsation. The 
boundaries of the heart arc normal, or but slightly increased; the 
sounds arc clear. The epigastric pulsation is, in Hamburger's 
opinion, due to the descending aorta and not to the right ventricle. 
The lability of the pulse is shown, on the one hand, by a rapid 
increase in the rate on sitting up, standing, and on slight physical 
exertion; and on the other hand, by sinus arrhythmia, increasing 
with inspiration and diminishing with expiration. This symptom 
is most marked in severe cases, but also occurs in normal children. 
Among the subjective circulatory symptoms are headache, similar in 
unset to migraine, but involving both sides of the head, usually in 
the occipital region. Sudden local anemias of the brain cause 
dizziness and unconsciousness, these symptoms and the headache 
being due not to a general anemia, as is often supposed, but to 
changes in the vasomotor system. A tendency to cold hands and 
feet is another symptom of this class, and also the above-mentioned 
cardiac pains due, according to Nbthnagel, to an ischemia of the 
heart muscle. Among the object ire circulatory signs are noted flush- 
ing or paling on psychical disturbance, coldness of the extremities, 
dermographia, visible pulsation of the carotids, and increased ten- 
sion of the arterial walls in the radial and temporal arteries. Cer- 
tain forms of bronchial asthma probably belong to this class. There 
are, besides, a large number of symptoms occurring in combination, 
all of which can be traced back to a nervous irritability of the 
whole circulatory apparatus. 

'I he rigidity of the arterial walls in nervousness is marked in 
many cases, and generally all children with apparently "thickened" 
arteries are nervous. Normally, under six years, the pulse only, 
and not the arterial wall, is felt by the ringers; and not until the 
tenth year are the arterial walls frequently palpable. Pallor, espe- 
cially in school-children, is often attributed to anemia, whereas it 
may result from arterial contraction due to nervousness; such 
children commonly have dark rings under the eyes. Marked vaso- 
neurotic symptoms do not usually begin until about the seventh 
year, when the child begins to attend school. As etiological factors 
Hamburger attributes an inherited disposition and certain psychical 
and physical irritating or stimulating influences, such as fright and 
joy and autosuggestion on the one hand, and toxins on the other. 
The prognosis of the vasoneurotic condition is good if psychical 
causes can be discovered and avoided, and the child's disposition 
modified by good hygiene and intelligent mental training. 



VASCULAR CRISES 273 

A. number of the symptoms and signs which I [amburger describes 
are also met with in constitutionally hypotensive Individuals. 

The Treatment of Peripheral Spasm. Cramps in the Legs. 
Nocturnal cramps in the legs are of common occurrence in hyperten- 
sive disease. The patient is often suddenly aroused from hi leep 
by an intense muscular cramp of great severity. These cramps, 
which are a result of vasomotor spasm may sometimes be relieved 
by tightly tying a string, tape or handkerchief around the extrem- 
ity above the poinl of pain, or by rubbing the limb vigorously with 
stiff brushes. The inhalation qf amy] nitrite has in my experience 
not been very satisfactory, and immersion of the extremity in hot 
water is usually no1 feasible because the cramp is generally over 
before the water can be obtained. As a remedy for chilblain*, 
Raynaud's disease and other conditions due to vasomotor ataxia, 
Brunton advises the use of the salicylates either with or without 
the bromides. He has also seen good results follow the adminis- 
tration of thyroid extract in small doses. (See Treatment of 
Arterial Hypertension, p. 310.) 



18 



CHAPTER XII. 

ARTERIAL HYPERTENSIVE CARDIOVASCULAR 
DISEASE, NEPHRITIS, Etc. 

Blood-pressure variations of from 10 to 30 mm. Ilg., and 
perhaps more, may be purely physiological in their nature. We can 
draw conclusions of the import of pressure variations only if they 
exceed these amounts, or if they are more or less regularly encoun- 
tered in the same individual. A systolic pressure constantly above 
160 mm., <ir a diastolic pressure constantly above 100 mm. Ilg., is 
definitely pathological at any age. The younger the subject with such 
a pressure the more abnormal must it be considered. Before middle 
life 145 mm. should not be exceeded. The pathological range of the 
diastolic pressure is much less than that of the systolic. 

Arterial sclerosis is often very variable in its distribution. As 
an example, the tendency for syphilis to involve the ascending 
aorta may be mentioned. Extreme degrees of nodular peripheral 
sclerosis often occur without corresponding involvement of the 
splanchnic vessels, and, on the other hand, severe renal vascular 
lesions may be associated with only moderate peripheral thicken- 
ing. Palpation of the radial artery is therefore not a procedure by 
which we can estimate the seriousness of arterial degeneration, nor 
is the absence of an accentuated aortic sound — although this is 
usually present — an indication that arterial pressure is not increased. 
The view that peripheral arteriosclerosis and cardiac hypertrophy 
are secondary to hypertension is constantly receiving corrobora- 
tion. It is therefore quite erroneous to speak of "hardening of the 
arteries" as the cause of increased blood-pressure, since it is the 
latter which is the cause of the former. 

The height of the diastolic pressure is often more important than 
that of the systolic tension. The former is far less subject to tem- 
porary variation and it further indicates the resistance which the 
heart has to overcome. It is also more of an index of the mean 
pressure than is the systolic pressure. A constant diastolic pressure 
of or above 100 nun. indicates hypertension regardless of whether 
the systolic pressure be 180 or 1 10 mm. 



THE CARDIAC OVERLOAD IS II Y 1'E RTEX SJO.X 



PLETHORA AND ARTERIAL HYPERTENSION. 

Plethora, a term applied to an increase in the total amount of 
the blood, was formerly supposed to be a frequent if no1 invariable 
accompaniment of arterial hypertension. The clinical manifesta- 
tions of this condition are described as consisting in peripheral 
congestion of the capillaries, dilated venules, a large volume pulse 
and bulging of the supraclavicular fossa', a clinical picture which 
earlier physicians not always unwisely perhaps construed as an 
indication for phlebotomy. Starling states thai the total blood 
volume is affected not only by the oxygen tension of the respired 
air, but also by the blood-pressure. 1 Recent experiments have, 
however, shown thai changes in the blood volume in artificially 
induced hypo- or hypertension are insignificant, and recenl studies 
in patients with nephritic hypertension have shown thai the total 
blood volume is normal if not actually subnormal. 2 

THE CARDIAC OVERLOAD IN HYPERTENSION. 

Under normal conditions one often finds the systolic pressure 
about 120, the diastolic pressure about 80, the pulse-pressure, 
therefore, 40. "Thus the amount of energy expended in maintain- 
ing the circulation in excess of that required to open the aortic 
valves and overcome the resisting pressure of SO, is 40. 'Die nor- 
mal load may therefore be considered s!!, or .">() per cent, of the 
diastolic pressure" (Stone 3 ). Applying this conception to hyper- 
tension it is apparent that a systolic- and diastolic pressure of 170 
and 100 mm. respectively yielding a pulse-pressure of 70 would 
furnish a heart load of tW (70 per cent.), or an overload of 20 per 
cent. Stone's studies indicate that while the clinical symptoms of 
hypertension generally do not appear until the overload exceeds 
25 per cent., and while with a modification of the habits of life 50 
per cent, may be borne, yet with an overload of 50 per cent, myo- 
cardial exhaustion may be precipitated by any sudden strain. 
Cadbury 4 found that as the cardiac load increased, decompensation 
became more frequent in his series of 305 hypertensive cases. With 
a load of 100 per cent, or more, 66 per cent, of the cases had broken 

1 Starling, E. G.: Human Physiology, 1915, p. 857. 

2 Keith, N. M., Rowntree, L. G., and Geraghty, J. T.: A Method for the Deter- 
mination of Plasma and Blood Volume, Arch. Int. Med., October, 1915, p. 547. 

3 The Clinical Significance of High and Low Pulse-pressures with Special Refer- 
ence to Cardiac Load and Overload, Jour. Am. Med. Assn., 1913, lxi, 1256. 

4 Studies in Blood-pressure, Arch. Int. Med., 1916, xviii, 317. 



276 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

compensation. T have not found the pulse-pressure percentage of 
the diastolic pressure, "the cardiac load," of any value in the esti- 
mation of circulatory efficiency. 

THE SIGNIFICANCE OF HYPERTENSION. 

Given a patient with a well-marked hypertension (190 mm. 
systolic and 1 10 nun. diastolic) \vc arc de facto warranted in assum- 
ing that the patient is suffering from Bright's disease, at least until 
further investigation has shown that the hypertension is due to 
some other cause. Authenticated cases, substantiated by autop- 
sies arc on record in which the kidneys of such cases have been 
entirely normal, but such instances are the exception. 1 To what 
tlif rise of pressure in such cases is due has not been satisfactorily 
explained, but arteriosclerosis alone without some renal involve- 
ment rarely, if ever, produces hypertension. The absence of albu- 
min and casts does not necessarily exclude disease of the kidneys; 
furthermore, repeated and careful urine examinations will often 
show characteristic findings in cases which, on a few examinations, 
may yield negative results. It is of vital importance that nephritic 
changes be discovered early, and therefore an arterial pressure 
disproportionately high in relation to the age of the individual 
always calls for careful investigation, not only by means of the rou- 
tine urine examinations but also, if possible, by some of the func- 
tional renal tests, preferably phenolsulphonephthalein. It should 
be remembered that in the early stages increased blood-pressure 
may be only intermittently present. The normal physiological 
causes -which raise arterial tension in nephritic cases produce an 
exaggerated response. In the later stages of the disease, when the 
cardiovascular system is weakening, the pressure often falls, but 
such a fall is generally coincident with the appearance of untoward 
symptoms and physical signs — dyspnea, vertigo, palpitation, a 
diminished urinary output, edema, etc. These occurrences may also 
be brought about if a high pressure be forcibly reduced by means of 
the nitrites; indeed, uremia may thus be precipitated. 

No definite general rules can be laid down for the prognostic 
or therapeutic import of a fall or a rise of blood-pressure. The 
significance of such an event depends both on the nature of the 
disease and on the state of the patient. In patients seriously ill 

Krehl: Oeber <!i'' krankhafte EBrhdhung dea arteriellen Druckcs, Deutsch. med. 
Wchnschr., 1906, xxi, 1872. Schlayer: Qntersuchungen ueber d. Funktion krankon 
Nieren, Deutsch. Arch. f. klin. Med., 1911, oii, 371. 



THE SIGNIFICANCE OF HYPERTENSION L'77 

a rise may indicate improvement, whereas the same Ending in a 
case of arteriosclerosis or nephritis maj mean thai uremic mani- 
festations are impending. Again, in the case of cardiovascular 
disease, increase of pressure may indicate better compensation and 
elimination and be associated with general improvement. A fall 
of pressure, however, may also be a harbinger of good omen as 
indicating a lessening of toxic products, carbon dioxide accumu- 
lation, and peripheral vasoconstriction the class of case which 
Sahli lias described as "high-pressure stasis." The fall of pressure 
just alluded to ma\ lie merely a fall of the systolic pressure or 
such a fall associated with an increase of the pulse-pressure, which, 
were it always demonstrable, would afford an easily comprehensible 
explanation of the physical improvement. Such is, however, bj 
no means always the case. Some cases show marked impm em< nt 
coincident with a decrease of both maximum and pulse-pre ure. 
Capillary pressure, upon which nutrition depends, does no1 varj 
directly with arterial pressure, bul is rather dependent upon the 
state of the arterioles and the veins. High pressure is no1 neces- 
sarily associated with a good, nor low pressure with a poor, circula- 
tion in the capillaries, [f the arterioles are contracted the arterial 
pressure, however high, fails to reach the capillaries. 

Classification of Arterial Hypertension. A satisfactory classifica- 
tion of arterial hypertension cannot be made until our knowledge 
of the etiological factors is more complete, but certain types are 
more or less well differentiated. Arterial hypertension is met with 
in association with: 

1. Demonstrable nephritis, as evidenced by urinary findings, 
retinal lesions, cardiac hypertrophy and accentuation of the aortic 
second sound. 

2. Demonstrable arteriosclerosis as indicated by radial thickening 
(leathery arteries), tortuosity of the temporal arteries, cardiac 
hypertrophy, retinal arteriosclerosis (front-piece). Syphilis is the 
common cause of this type. 

3. A combined type in which both renal and arterial lesions are 
manifest. 

4. Non-nephritic hypertension (essential hypertension). — Regard- 
ing this variety of the disease, if the hypertension of polycythemia is 
excluded, there is great difference of opinion. 

Some authorities hold that latent glomerulonephritis is the cause 
of the increased blood-pressure ; others maintain that it is a distinct 
pathological entity due to some as yet unknown and probably 
chemical cause, such as auto-intoxication or abnormality of endo- 
crine secretion. 



278 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

Riesman 1 whose classification lias just been given, emphasizes 
the importance of recognizing a variety of non-nephritic hyper- 
tension occurring often in women past middle life, who are obese, 
undersized, ruddy complexioned and possessed of considerable men- 
tal and physical energy, without demonstrable arterial or renal 
abnormalities. The nun of this group are apt to be deep-chested, 
robust and great expendors of energy. Obesity is per se not infre- 
quently associated with arterial hypertension. Among 59 cases 
without apparent renal or vascular disease, 16 showed pressures 
between 1 15 and L60 nun., between 165 and 180, and 4 between 
L85 and 250 nun. Ilg.- 

This class represents a large and important group of hypertension 
cases but many of them die a nephritic death, although this may not 
occur for many years after the onset of the increased pressure. 
The writer is of the opinion that many of these cases are due to a 
latent nephritis, but that certainly all of them are not. In the 
essential hypertension cases the blood-pressure is generally lower 
in both its phases than in the nephritic group. It is also more 
amenable to treatment. As a rule the dietetic treatment of these 
eases may be much more liberal than in the nephritic group. 

The Symptoms of Arterial Hypertension. — Cardiovascular Symp- 
toms- Dyspnea, palpitation, vertigo, oppression — often on going 
to bed — cardiac erythism, angina pectoris, muscular cramps, spon- 
taneous or on exertion, edema of lungs, arrhythmia. 

Renal Symptoms. — Polyuria, with nocturnal micturition — the 
urine having a low specific gravity and containing a few hyaline 
or granular easts and a trace of albumin. 

Gastro-inte.st/ual Symptoms.— 1 hspeptic manifestations with eruc- 
tations, flatulence, postprandial discomfort, hyperacidity, constipa- 
tion, epigastric pain, tenderness, or oppression. 

Nervou* Symptoms. — Matutinal headache, 3 nervousness, restless- 
ness, irritability, inability to concentrate, easy fatigue from mental 
exertion, insomnia, numbness, tingling, migraine, transitory aphasia, 
hemiplegia, apoplexy. 

Ocular Symptoms. — (a) Spasmodic symptoms, without definite 
anatomical lesions: amblyopia, transient amaurosis, hemianopia. 

(h) Constant symptoms, with increased pressure of cerebrospinal 
and cerebro-arachnoid fluid. They tend to be progressive and may 

1 Arc We Exaggerating the Dangers <>f Arterial Hypertension, Penn. Med. Jour., 
I December, 19] I. 

i : [Jgeskrifl f. Laeger, 1915, lxxvii, No. 23. 
I "i detailed description mid discussion <>f these headaches Bee Renon, L.: La 
( !epha!6e matinale continue des Hypertendus, Pariam£ dicale, L916, \i, I. 



the sk, mficaxch or ii)i'i:irn:\sm\ 279 

load to subconjunctival or retinal hemorrhages, glaucoma, etc. 
(See page 131. 1 

Aural Symptoms- Tinnitus annum, either with or without 
vertigo. (See page 269.) 

It frequently happens that the subjects of arterial hypertension 
complain only of respiratory or gastro-intestinal symptoms. Unless 
blood-pressure elevation and cardiac hypertrophy are soughl for 
by the examiner the true etiological factor i^ apt to be overlooked, 
[ndigestion, bloating after meals, slight dyspnea on exertion, and 
nocturnal micturition arc very suggestive manifestations. Such 
individuals arc usually overweight overfed and underexercised 
especially in the case of men who have a plethoric, robust appear- 
ance. But hypertension also occurs in abstemious individuals, and 
in such seems to bear a very frequent relation to overwork, worry, 
and insufficient relaxation. According to Volhard,' the Japanese 
are rarely the subjects of arterial hypertension, a fact which suggests 
that diet and mode of life may account for their relative immunity. 
Severe or recurrent epistaxis is sometimes associated with and due 
to arterial hypertension and in such cases may act beneficially in 
reducing the pressure. 

Physical Signs. — Heart. — Hypertrophy chiefly left-sided, accent- 
uation, splitting or reduplication of the aortic second sound; later, 
systolic murmurs at the mitral or aortic areas are often found. 
Cardiac or aortic dilatation, arrhythmia generally extrasystolic 
or when compensation fails, auricular fibrillation; bradycardia, 
rarely pulsus alternans. 

Arteries. — Flushing and duskiness of the face and hands; a hard, 
relatively incompressible pulse. Cervical pulsation, prominent 
and tortuous superficial arteries (temporal, brachial, femoral), 
arterial sounds. Retinal vascular sclerosis, rhythmic movements 
of the head (pulsatile), arcus senilis. 

In most of the cases high blood-pressure is mainly the result 
of vascular spasm. Thus, for example, there may be relatively 
normal bloodvessels with marked vascular contraction; or distinct 
fibroid changes with moderate spasm. Marked lability of blood- 
pressure is common. We have seen that in health pressure varia- 
tions are constantly brought about by diverse influences. In 
arterial hypertension all such responses are exaggerated, and 
although arteriolar pressure is high, capillary pressure is low. 
Intercurrent infections generally cause a temporary fall of pressure. 

1 Ueber d. funktionelle Unterscheidung der Schrumpfnieren, Kong. f. inn. Med., 
xxviii, 735. 



280 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

When high pressure has been long standing one frequently finds a loss 
of vascular compensation which results in a lowering of pressure, 
simply because the arterial musculature is no longer able to maintain 
a high degree of tonicity. The arteries become relaxed, tortuous, 
stretched, and are prominent on inspection. Such a break in vascular 
compensation may temporarily give relief to an overburdened heart, 
but usually does so at the cost of general nutrition and sometimes 
precedes a progressively downward course from insufficient renal 
activity. Such a broken cardiovascular compensation accounts 
for the secondary fall of pressure often seen in the late stages of 
arteriosclerosis. 

The exact mechanism which leads h> dilatation of the arteries is still 
uncertain. The transplantation of sections of a vein into an artery, 
after the method of ( arrel, does not lead to a dilatation of the 
vein, despite the greater pressure to which it is, in its new situation, 
exposed; in fact, a thickening and decrease in caliber results. 
This fact would indicate that " increased blood-pressure cannot in 
itself produce a lasting progressive dilatation of the bloodvessel." 1 

Moderate pressures are naturally better borne than very high 
ones, and as a general rule ambulant patients with constant pressures 
of 170 mm. are in no immediate danger. A systolic tension of 200 
nun. and over, however, renders sudden catastrophies not unlikely, 
although such cardiovascular strains may be borne for eight to 
ten years (see p. 136). 

Arterial hypertension is more common in men than in women, 
but high pressures are generally better and longer endured by the 
latter, owing to their more ready adaptability to a restricted life 
and to their lessened' exposure to sudden hypertensive influences. 

In some eases of hypertension marked slowing e>f the pulse is a 
striking clinical feature which, in the absence of local cardiac 
disease of the conductive system, is due to the fact that hypertension 
stimulates the cardio-inhibitory centre. This inhibitory action is 
brought about either by the direct effect of increased pressure 
in the vessels supplying the cardio-inhibitory nerves, or reflexly 
by stimulation of the peripheral nerves in the vessels. Increased 
pressure in the left ventricle has little effect, but in the thoracic 
aorta the effect is more marked. This reflex stimulation may 
disappear while the effect of direct pressure on the bloodvessels 
of the cardio-inhibitory centre still remains. 2 

I ischerand Schmieden: Frankfurt Ztscbr. f. Path., 1909, Hi. 8. 

i and Hooker: Slowing of the Pulse from Increased Blood-pressure, Am. 
.I..,,,. Physiol., 1908, xxi, :<7:i. 



NEPHRITIC ID n.HTENSlON 281 



NEPHRITIC HYPERTENSION. 



The increased blood-pressure which occurs in connection with 
renal disease, especially with that form \\ hich fe clinically designated 
as chronic interstitial nephritis, is the I striking and diagnostic- 
ally perhaps the most important abnormality "I' arterial ten inn 
which is met with in the entire domain of medicine. There eems 
to be a tendency to revert to the old concepl of Gull and Sutton, 
to the effect that chi-oiiic interstitial nephritis results from general 
and not merely local disease of the arterioles thai it is primarily 
a vascular disease of which the renal changes are bul secondary 
manifestations. Certainly it is a fact that the clinical pictures 
as well as the blood-pressure findings of chronic interstitial nephritis 
are quite dilleivnt from those seen in the "parenchymatous" 
variety of renal disease. Whether the rise of blood-pressure occurs 
before structural vascular lesions exisl is still in question. The belief 
that it does has been put forth by von Basch "angiosclerosis"), 
by Huchard ("presclerosis"); and by Allium ("hyperpiesis"). 

Hyperpiesis. — The term hyperpiesis has been applied to hyper- 
tension not due to demonstrable renal, cardiac and arterial disease. 
It is suspected that if unchecked this condition may be an ante- 
cedent of organic hypertension. In arteriosclerotic conditions the 
increased blood-pressure, at least up to a certain point, subserves 
a necessary purpose; in hyperpiesis, so far as we can determine. 
the pressure increase in addition to being sudden and associated 
with unpleasant symptoms subserves no useful function. 

Glomerulonephritis. — The recent studies of Volhard and Fahr 1 
have emphasized the fact that blood-pressure is increased in diffuse 
glomerulonephritis regardless of whether the condition is acute, 
chronic or in its terminal stage, whereas simple degenerative 
nephritis (parenchymatous nephritis) — disease of the epithelial 
tubules — is not associated with hypertension. In the interval 
between the acute and the terminal stage of glomerulonephritis, 
increased blood-pressure, together with slight albuminuria and 
occasional casts are the only signs of Bright's disease, other renal 
tests showing normal results. 

Simple Renal Sclerosis. — The highest blood-pressures are often 
met with in renal arteriosclerosis, in cases in which the intima of 
the smallest renal arterioles is thickened and in which only occasional 
glomeruli or tubules show abnormalities. This condition has been 

1 Die Brightische Nierenkrankheit, Berlin, 1914. For an excellent resume see 
Austin, J. H., Prog. Med., 1915. 



282 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

termed simple or benign sclerosis, since it is compatible with many 
years of useful life. This type of renal disease corresponds to Gull 
and Sutton's primary vascular disease. Its close connection with 
the heart both in its symptomatology and mode of termination 
(cardiac failure) has led Janeway to suggest the term cardiovascular 
hypertensive disease. Ten to 15 per cent, of these cases, however, 
insidiously develop renal symptoms such as albuminuric retinitis, 
decreased phthalein elimination, polyuria, or increased non-protein 
or urea nitrogen in the blood. Such cases clinically and sometimes 
histologically represent a combination form of the simple sclerotic 
and the glomerulonephritic types. 

In this type of renal disease cardiac hypertrophy is marked, 
especially if the arterial changes in the kidney begin early in life. 
When developed later in life the frequently associated coronary 
sclerosis renders cardiac hypertrophy less readily possible. Among 
268 eases studied by Yolhard and Fahr, 102 had a systolic pressure 
above 200 mm.; 104, between 170 and 200 mm., and only til 
pressures below 170 mm. 

Renal Sclerosis. Glomerulonephritis. 

Age, forty to fifty years. Age, twenty to fifty years. 

More frequent in women. More frequent in men. 

Apparently well nourished, often obese, Appearance: sallow, icteroid, emaciated; 

fair color, not anemic; digestion good. tense, prominent vessels, anemia, 

gastro-intestinal disturbances, ammOr 
niacal odor on breath. 

Blood-pressure often very high. Blood-pressure high. 

Retinal lesions: hemorrhages, but no Retinal pictures: hemorrhages, albumi- 

albuminuric retinitis. auric retinitis. 

Phthalein normal. Phthalein diminished. 

Blood nitrogen normal and not abnor- Blood nitrogen increased, headaches, 

mally increased by protein feeding. vesical disturbances, nausea, vomit- 

Cardiac hypertrophy often marked ing. 

with circulatory embarrassment, 

slowly progressive. 

Death generally from heart failure. Death often in uremia. 

Symptoms. — The symptoms of functional hypertension may be 
any of those seen in the organic variety. The pressure readings 
associated with such symptoms are characterized by their lability, 
the exacerbations of pressure being evidently spastic in origin. 
Hyperpiesis occurs in men after middle life, and in women at the 
time of the menopause (see page 418). A disturbed balance between 
the organs of internal secretion, especially the thyroid, the adrenals 
and the sexual glands, has been suggested as a possible cause. 

In the vast majority of cases a systolic blood-pressure of over 
Kill nun. and a diastolic pressure of over 100 nun. if constantly 



NEPHRITIC ll) PERTENSION 283 

present, points indubitably to thai symptom-complex which i 
designated as interstitial nephritis, especially if it. be associated 
with polyuria and urinarj abnormalities. It dues no1 Qece aril; 
mean, of course, that the individual in question will die of uremia 
or dropsy, for manj cases succumb to cardiac or vascular lesions. 
Occasionally cases are encountered in which practically normal 
kidneys are found at autopsy, but as a genera] rule the small red 
atrophic organ is found. Many forms of renal disease are associated 
with a slightly increased blood-pressure, the notable exception 
being degenerative {tubular) nephritis, amyloid disease, suppurative 
pyelonephrosis, and tuberculosis. 

Arterial hypertension is generally a condition of gradual develop- 
ment extending over years of time, with a tendency to increase, 
and with period- of spontaneous intermission or exacerbation. 
These latter are often, hut h\ no means alwa\ s, t raceable to h\ gienic 
or dietetic variations. They are very closelj associated with 
psychic phenomena which are generally by far the most potent 
factors for good or ill. 

The degree of tension which can be borne without subjective 
consciousness is mainly an individual question, hut a pressure of 
180 mm. is not often exceeded without symptoms, and constant 
pressures of 200 mm. or over are generally not Inn- maintained 
before leading to some sudden catastrophe, such as angina pectoris, 
uremia, or apoplexy. The significance a- will a- the seriousness 
of high blood-pressure often receives useful elucidation a- the 
result of an ophthalmoscopic examination. 

Etiology. Volumes have been written based upon clinical and 
pathological findings, upon theoretical considerations, and upon 
experimental evidence to account for nephritic hypertension since 
1836, when Richard Bright 1 described the disease which now bears 
his name, and suggested as a cause of the cardiac hypertrophy 
which occurs in many cases, even in the absence of valvular disease: 
(1) "That the altered quality of the blood affords irregular and 
unwonted stimulus to the organ immediately," or (2) "that it 
so affects the minute and capillary circulation, as to render greater 
action necessary to force the blood through the distant subdivisions 
of the vascular system." 2 The subject, which cannot be exhaustively 

1 Jores found that the absence of hypertrophy in advanced interstitial nephritis 
is usual in the form known as the secondary contracted kidney. In the typical red 
granular kidney hypertrophy is the rule, with, however, occasional exceptions, 
Verhandl. d. deutsch. path. Gesellsch., 1908, xii, 187. 

2 Bright, R.: Cases and Observations Illustrative of Renal Disease Accompanied 
with the Secretion of Albuminous Urine, Guy's Hosp. Repts., London, 1836, i, 338. 



2S4 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

discussed here, has recently been most ably reviewed by Ja noway, 
from whose article 1 have freely drawn. 1 

It is now generally believed that the cardiac hypertrophy is in 
nearly all cases due to arterial hypertension, and to explain the 
cause of the latter a number of hypotheses have been offered. 









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»*^^SSw»S^'d^^x^?^?75^t?--^-r >SbH 








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Hsb*i?*". 


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Fig. 97. Photograph of 



>f a normal kidi 
i ( rhoreyeb.) 



jhowi 



vascular supply. 




I ig, 98. The vascular supply in slight diffuse nephropathy. (Ghoreyeb.) 

1. Mechanical Theories. The old mechanical theory of Traube, 
which attributed the hypertension to resistance in the kidney itself, 
and which had almost fallen into oblivion (since ligature of the 



'Janeway, T. C: Nephritic Eypertension, Clinical a 
Am. Jour. Med. Sc, 1913, cxlv, 625 (bibliography). 



Experimental Studios, 



\i:riii:iTic liYi'F.ia'i-issios 



285 



penal vessels docs not produce an increase of blood-pressure), lias 
recently been rejuvenated. Katzenstein has reported that in a 
dog constriction of the renal arteries, without complete obliteration, 
leads to an increased pressure. These results were no1 corroborated 
by others. Thus Alwens, 1 by placing the kidneys in an oncometer 




Fig. 99. — The vascular supply in chronic diffuse nephropathy with atrophy, 
(Ghoreyeb.) 




Fig. 100. — Vascular cast of a tuberculous kidney. (Ghoreyeb.) 

without touching the vessels, on increasing the pressure 2 or 3 mm. 
Hg. above the arterial tension, found that blood-pressure in the 
aorta rose and was maintained as long as renal compression con- 



1 Experimentelle Untersuehungen u. d. Bedeutung d. meehanischen Theorie d. 
nephritischen Blutdrucksteigerung, Deutsch. Arch. f. klin. Med., 1909, xcviii, Nos. 
2 and 3. 



286 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

tinued. But in these experiments the flow from the renal vein 
was diminished, almosl suppressed, a fact which renders the experi- 
ment incomparable to nephritis, in which no such obstruction to 
venous outflow exists. Embolization of the kidney with paraffin, 
as practised by Muller and Maas, did not increase blood-pressure. 
The blood flowing through the kidneys under normal and under 
increased pressure generally shows no increase in How, "even at the 
time when very pronounced rises in arterial pressure had developed" 
Burton-Opitz and Lucas). 1 

The constriction of the arterial bed which is associated with some 
forms of renal disease has been objectively demonstrated by 
( rhoreyeb's 2 metallic casts of the renal vascular system. 

Loeb 8 demonstrated the fact that the degree of arterial hyper- 
tension bore a more or less definite relation to the degree of glo- 
merular renal involvement, and suggested that the increased pressure 
was a reflex compensatory effort of the system—an attempt to 
supply, by means of splanchnic constriction, an adequate blood- 
supply which local vasodilatation alone was no longer capable of 
furnishing. This attractive hypothesis has, however, been proved 
incorrect by -lores and others, who have shown that glomerular 
changes were often conspicuously slight when blood-pressure was 
highest, and vice versa. Furthermore, as has been recognized 
by many, and emphasized by Janeway, "amyloid disease, 
which is par excellence a disease of the glomeruli, in its pure form 
is almost invariably without effect on the blood-pressure, and 
without an accompanying hypertrophy of the heart. This fact 
is one of the most difHcult to be reconciled with any theory of 
nephritic hypertension." 

II. Chemical Theories.— -The chemical hypothesis attributes the 
increased blood-pressure to substances in the blood as resulting 
from either (1) insufficient renal elimination; (2) disturbances of 
internal secretion; (3) toxic substances set free by the diseased 
kidney. 

Following the suggestion of Bright, that an altered composition 
of the blood might account tor the cardiovascular changes, it was 
for a time believed thai hypertension was due to retained toxic 
products which the kidneys failed to eliminate, which produced first 
Spastic hypertension and later arteriolar hypertrophy. 

'.!„ur. Exp. Med., 1911, riii, 308. 
3tudies on the Circulation. Jour. Med. Research, 1916, xxxv, 87. 
i,i„r .1. Blutdruck u. Berzhypertrophie bei Nephritikern, Deutsch. Arcn.f. 
kliu. Med., 1905, bocxv, 348. 



\ EPHRITIC II) PERTENSION 287 

If after removing one kidnej from ;i dog, portions of the remain- 
ing kidney (not exceeding two-thirds of the total kidney substance 
be resected, the animals after developing polyuria ultimately die 
of cachexia. I ; i\ e among eighteen dogs upon whom these graduated 
nephrectomies were practised by Paessler and Heineke 1 showed 
an average blood-pressure increase of 21.5 nun., together with 
left ventricular hypertrophy. They found thai after destruction 
of a certain amount of kidney substance the quantity of urine 
increased, but was poor in extractive substances, especially the 
aitrogenous elements which tended to accumulate iii the blood 
and the tissues. The same phenomena perhaps occur in nephritis, 
hut they do not manifest themselves for a long time. There is a 
polyuria at the beginning; later extractive substances are eliminated 

in diminished quantity; finally, nitrogen accumulati :curs in 

the blood and tissues, forming whal is designated ;i-. the products 
of nitrogen retention. 

Paessler states that (a) cardiac hypertrophy in nephritis is due to 
the renal disease; (b) as a result of the latter there occur- an 
increased stimulability of the vasoconstrictors causing spastic con- 
traction of the arteriole-; (c) that right-sided cardiac hypertrophy 
is secondary to left ventricular failure. These graduated nephrect- 
omy experiments leading first to hypertension, polyuria, and albu- 
minuria, and later to gastro-intestinal disturbances, cachexia, 
hypotension, and death, have been corroborated by Pearce 2 and 
Janeway. 3 The exact mechanism by virtue of which this hyper- 
tension is produced is still uncertain, but it is in all probability due 
to increased arterial tonus. It has been found experimentally that 
in gradually nephrectomized animals, arterial spasm is brought 
about by stimuli which in normal animals are insufficient to engender 
similar results. It must be borne in mind, however, that " although 
the results of reduction experiments are striking, the procedures by 
which they are obtained are not such as to involve only a single 
factor, but bring several forms of kidney injury into play; that is, 
reduction of functional substance and productive atrophic and 
vascular changes, accompanied by the elimination of albumin and 
casts" (Pearce). 

1 Versuche z. Pathologie d. Morbus Brightii, Verhandl. d. deutsch. path. Gesellsch., 
1905, ix, 99. 

2 The Influences of the Reduction of Kidney Substance upon Nitrogenous Metab- 
olism, Jour. Exp. Med., 1908, x, 632; A Study of Experimental Reduction of Kidney 
Tissue with Special Reference to the Changes in that Remaining, ibid., 1908, x, 745. 

3 Note on the Blood-pressure Changes following Reduction of the Renal Arterial 
Circulation, Proc. Soc. Exp. Biol, and Med., 1909, vi, 109. 



288 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

Ten cases of high-grade hypertension were studied at autopsy 

by Ilerxheimer. 1 In no ease was the parenchyma of the kidney 
microscopically normal, but in most cases the changes were small 
in comparison with the constant high-grade arteriosclerotic vascular 
degenerations, especially of the arterioles. In all ten cases extensive 
hyaline thickening and fatty degeneration of the intima occurred. 
Slight or complete obliteration of the lumen was found. In some 
cases especially the vasa atl'erentia of the glomeruli were involved, 
and also some loops of the glomeruli showed the fatty and hyaline 
degeneration. In addition, atrophy of the tubules, increase of 
connective tissue, infiltration of round cells were noted (the vascular 
changes of the old Gull and Sutton arteriofibrosis) ; in the other 
organs, in opposition to Jores's findings, there were only occasional 
vascular changes (in the pancreas, testicles, liver, and always much 
less extensive than in the kidney). Only in the spleen were vascular 
changes constantly found, but among 410 spleens examined there 
was in 170 marked hyaline change in the intima of the small vessels, 
even in young people, so that the findings in the spleen have no 
particular weight. 

It seems, therefore, that although general arteriosclerotic changes 
occur, they are more marked in the kidneys than elsewhere, and that 
the arterial changes arc flic cause, nut the result, of the arterial hyyer- 
t> ns ion. 

lien in. — Retention of ordinary metabolites, such as urea, does 
not explain arterial hypertension, and many attempts have been 
made to identify pressor substances in the blood. Tigerstedt 
and Bergmann succeeded in extracting from a rabbit's kidney a 
substance (renin) which experimentally increased arterial tension 
when injected into animals. It has been suggested that autolysis 
of the diseased kidney causes this substance to be thrown off into 
the general circulation. 2 Ascoli found that nephrotoxic serum 
possessed hypertensive properties, while Riva-Rocci and Marag- 
liano obtained a similar substance in increased quantity in the 
diseased kidney. While those findings have been widely quoted, 
Pearce 3 has definitely shown that nephrotoxins are not truly specific, 
that "the production of autonephrolysin by injuring one kidney 
was doubtful, and that Ascoli's claim of a blood-pressure-raising 
substance could not be confirmed." 

1 Niereund Bypertonie, Verhandl. d. deutsch. path. Gesellsch., 1912, xv,S. 211-216. 

'Shaw, H. B.: Auto-intoxication; its Relation to Certain Disturbances of Blood- 
pressure, Goulstonian Lectures, Lancet, 1900, i, 1295, 1375, 1455! 

3 The Theory of Chemical Correlation as Applied to the Pathology of the Kidney, 
Arch. Int. Med., August, 1908. 



\ EPHRITIC ID PERTENSION 

Pence 1 has shown experimentally that a dog's kidney, unlike 
that of a rabbil and certain other animals, does not contain a 
depressor substance. Of course il doesnol follow thai there nil in 
human aephritis run parallel with those of experimental nephritis, 
but a comparison is, to say the least, interesting. 

Moreover, the injection not only of saline kidnej extract bul 
also that of other organs except the adrenal, pituitary, and spleen, 
has failed to increase blood-pressure, 2 and last, although by no 
means least, "hypertension is mosl extreme in those ii 
chronic types of nephritis in which breaking down of kidney sub- 
stance must he nt a min imum if there is any at all" (Janeway). 

Epinephrin. Although first suggested 1>.\ Neusser, the hypothesis 
that nephritic hypertension is due to increased activity of the 
suprarenal glands was prominently brought to the fore by Vaquez 3 
and the main exponents of this doctrine are till to he found in 
France. 

Marcuse believes that as the result of the resistance thus opposed 
by the kidneys to the circulation an enlargement of the inferior 
suprarenal artery, a branch of the renal artery, occur-. The supra- 
renal gland being thus oversupplied with blood secretes an ii i 
quantity of epinephrin. The objection to this explanation lies 
in the fact that the inferior suprarenal artery is often lacking or, 
when present, is not given oil' From the renal artery. 

From an experimental stand-point it seems well established that 
there exists a definite physiological antagonism between pancreas 
extract and adrenalin, regarding their effect on blood-pressure in 
normal animals. Zondek 1 has recently shown that pancreas extract 
exerts its usual hypotensive effects after the production of experi- 
mental nephritis. An injection of pancreas extract is capable of 
completely neutralizing increased blood-pressure in uranium and 
mercurial nephritis, but fails to do so in the case of chromium 
lesions. 

Cow 5 has shown that a direct vascular connection exists between 
the adrenals and the kidney, and that a part of the glandular secre- 
tion passes directly into the kidney. When the adrenal vein is 
ligated enough epinephrin reaches the kidney to cause anuria. 

1 An Experimental Study of the Influence of Kidney Extracts and of the Serum 
of Animals with Renal Lesion on the Blood-pressure, Jour. Exp. Med., 1909, xl, 430; 
The Influence of Kidney Extracts on Blood-pressure, Arch. Int. Med., 1912. 

2 Miller, J. L., and E. M.: The Effect on Blood-pressure of Organ Extracts, Jour. 
Physiol., 1911, xliii, 242. 

3 Hypertension, Proc. Congres Francaise de Med., 1904, p. 338. 

4 Beeinflussung des Blutdrucks d. akuten Experiment ellen Nephritis d. Kannin- 
chens durch Pankreas extrakt, Deutsch. Arch. f. klin. Med., 1914, cxv, 1. 

5 Jour. Physiol., 1914, xlix, 443. 

19 



290 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

Although the epinephrinemia hypothesis is an attractive one, 
with certain facts to commend it, accumulating evidence points 

strongly to its fallaciousness. Thus it appears (1) that there is 
no constant relation between the degree or even the presence of 
hypertension and the anatomical structure of the glands. 1 (2) The 
results obtained by estimating the epinephrin content of the glands 
in different conditions are inconclusive. 2 (3) Most of the studies 
based upon the adrenalin content of the blood are faulty because 
of lack of controls — in order to be conclusive the test should respond 
to a frog's eye, coronary artery, and intestinal ring method, and, 
as Janeway suggests, show not only qualitatively typical but 
also quantitatively possible epinephrin effects. (4) Physiological 
evidence indicates that the adrenal glands are normally only 
intermittently active. They are emergency organs, but not con- 
stantly concerned with the maintenance of normal blood-pressure. 3 
All deductions based clinically or experimentally upon qualitative 
or quantitative analysis of adrenalin in the serum must be accepted 
with reserve. Chemical tests are out of the question, and biologi- 
cal tests such as the frog eye or muscle strips, are unreliable, since 
substances in the blood other than epinephrin may produce the 
reaction. 4 (5) The injection of epinephrin into the blood causes an 
increased glycemia which, if sufficient in amount, appears as 
glycosuria, and yet investigations upon patients with high arterial 
tension from the stand-point of hyperglycemia have shown indefinite 
results. 

Cholesterinemia. — An excess of cholestrol in the blood has also 
been credited by French observers, with causing hypertension. 
When fed to rabbits this substance is said to cause sclerosis of the 
aorta and adrenal hypertrophy associated with an excess of lipoids 
in the glandular cortex. But these results were not corroborated. 5 

There is some evidence that the rise in blood-pressure which is 

1 Pearce, K. M.: The Relation <>f Lesions of the Adrenal Claud to Chronic 
Nephritis and to Arteriosclerosis; an Anatomical Study, -lour. Exp. Mod., 1908, x, 735. 
Borbern: Das Chrnniafnne (lewclic. Nebonnioronuntorsuehunnen, Skand. Arch. 
f. Phys., 1912, xxviii, 91. (Abstr. Zentralbl. f. d. Cos. inn. Mod., 1913, iv, as.i. 

- Ingier and Schmorl: Ueber d. Adrenalingehalt. d. Nebennieren, Deutsch. Arch, 
f. klin. Mod., 1911, civ, 262. 

3 Trendelenburg, \\ . : Uohor d. Beziehungen d. Nebennieren z. normalen Blut- 
druckhdhe, ZtBchr. f. Biol., 1914, xliii, 155. Hoskins and McClure: The Adrenals 
and Blood-pressure, Arch. Int. Med., October, 1912, p. 343. 

* Stewart, C. N.: So-called Biological Tests for Adrenalin in the Blood, with Some 
Observations on Arterial Hypertonus, Jour. Exp. Mod., 1911, xiv, 377. O'Connor: 
I'rU-r .1. Adrenalingehall dea Blutes, Arch. f. oxp. Path. a. Pharmakol., 1912, Ixvii, 
L95. For other references see Janeway's article, loc. cit. 

» Dixon and Halliburton: .lour. Physiol., 1913, xlvii, 229. Cantieri, C: Rev. 
Crit. di Clin. Med., 1913, xiv, 657. 



\ EPHRITIC II) PERTENSIOh 291 

met with in nephritis may have a variable and composite cau e. 
Tims the injection of bovine pancreas extract into the circulation 
of rabbits suffering from experimental nephritis produces a fall of 
blood-pressure, but in uranium nephritis larger doses are required 
than in the chromic nephritides, while in the bichloride type of 
kidney only slight pressure changes occur. The subsequent rise of 
pressure also differs in that the uranium and bichloride pressures 
never again exceed the prenephritic level, whereas the chromic 
animals promptly rise to the previous high level. 1 

From what has preceded it is sadly evidenl that we are -till 
unable to satisfactorily explain either the cause or the mechanism 
of nephritic hypertension. The whole subjed is so complex and 
the evidence at hand so contradictory that judgment is difficult. 
Janeway, than whom no one i- better qualified to speak, draws 
the following conclusions: 

1. Hypertension may arise through purely quantitative reduction 
of kidney substance below- the factor of safety. It is difficult to 
conceive of this as other than a vascular hypertonus due to retained 
poisons of some kind. Its clinical paradigm is the hypertension 
accompanying bilateral ureteral obstruction or the unfortunate 
surgical removal of the only functionating kidney. Possibly it is 
one factor which helps to produce hypertension in the contracted 
kidney. 

2. Hypertension may arise in connection with the unknown 
intoxication which causes disturbances of the central nervous 
system, and which we call uremia. This intoxication is not one of 
retention, in a strict sense, although it is most commonly present 
in those cases of advanced nephritis which manifest marked nitrogen 
retention. Clinically it is associated with severe acute nephritis, 
sometimes at its very onset, besides the subacute and chronic 
inflammatory affections of the kidney. 

3. Hypertension may arise in primary irritability of the vaso- 
constricting mechanism from unknown, probably extrarenal, 
causes which lead eventually to arteriosclerosis. In this type the 
disease in the kidney is the sequence, not the cause, of the general- 
ized vascular lesion. When it progresses to a condition of extreme 
atrophy, resulting in the true primary contracted kidney, a renal 
element may be added to the existing hypertension. In some cases 
arteriosclerosis of the larger vessels may spread peripherally and 
produce a similar form of disease. In these forms of primary 

1 Zondeck, H.: Die Beeinflussung des Blutdrucks d. akuten exper. Nephritis d. 
Kaninchens durch Pankreas extrakt, Deutsch. Arch. f. klin. Med., cxv, Heft 1 and 2. 



292 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

vascular disease it is probable that eventually widespread narrow- 
big of the arterial stream bed in some cases produces a permanent 
organic increase in peripheral resistance. 

Vbegtlin and Macht 1 have succeeded in isolating from the 
blood and serum a crystalline pressor substance, whose pharma- 
cological action is different from epinephrin and from any other 
body hitherto obtained from the blood. It produces marked 
cardiac stimulation and a prolonged vasoconstrictor effect. They 
found that its physical and chemical properties seem "to point to 
its relation to cholesterin on the one hand and to the cortex of the 
adrenal gland on the other." Gtibar 2 has shown that the blood-serum 
of nephritics has a pressor effect and Cantieri 3 found that there 
was no relation between high blood-pressure and the cholesterin 
content of the blood. It is quite possible that this new substance 
may prove to be of considerable clinical importance. Occasionally 
hypertension is caused by focal infection, such as pyorrhea, sinusitis, 
chronic tonsillitis, suppuration in the antrum, etc., presumably as 
a result of toxin absorption and renal irritation. The relation of 
hypertensive cardiovascular disease to syphilis has been considered 
under the heading of the latter, p. 222. 

Renal Circulation and Function ation.- — Renal functionation is 
extremely sensitive to vascular changes in the kidney. The kidney 
differs from other organs of the body by functionating more or 
less constantly and by being frequently forced to do extra work by 
its possessor. According to Tiegerstedt, from ten to nineteen times 
more blood passes through the kidneys, despite their small size, 
than through all the other organs combined. 4 The kidney normally 
contains about 1.63 per cent, of the total blood (Ranke). During 
well-marked diuresis it may contain 5.6 percent. 5 The anatomical 
arrangement of the vessels insures the longest possible blood path, 
together with a double system of capillaries. The kidney may 
show an increased rate of blood flow without an increase either 
in volume or in pressure, a fact which I Iasebroek uses to substantiate 
his belief in an active vascular diastole. Renal activity is inde- 
pendent of general systemic pressure. 6 Vasoconstriction alone 
may cause a great reduction of blood flow in the kidney (B. Opitz). 

1 The Isolation of a New Vasoconstrictor Substance from the Blood and the 
Adrenal Cortex, Presence of the Substance in the Blood and its Action on the Car- 
diovascular Apparatus, Jour. Am. Med. Assn., 1913, lxi, 213G. 

- Russk. Vratch, 1913, xx, 725. » Wiener klin. Wchnscbr., October 16, 1913. 

4 Lehrbuch d. Physiologic dee Kreialaufes, Leipzig, 1893, p. 552. 
Landi rgren and Tigeretedt: Skand. Arch. f. Physiol., 1892, iv, 242. 
Weber: Arch. f. exp. Path. u. Phar., 1905. liv. 



NEPHRITIC HYPERTENSION 293 

The secretion of urine varies directly with the puhe-pressure. 1 
In fact, a marked increase of pressure may produce albuminous 
urine, and a decrease below a certain point causes anuria. 

It lias generally been believed that the circulation through the 
kidneys, as regards vascular dilatation or contraction, depended 

upon the amount of urogenous material in the Id I, and thai the 

secretion of urine increased with an increased blood-pressure and 
blood How. The increased pressure is believed to especially cause 

an excretion of water, the concentrati if the urine depending 

upon the activity of the renal epil helium. I [ypertension only causes 
a polyuria if the blood contains a definite am. unit of UTOgenOUS 
material. In case of atrophied kidneys with a restricted capillar} 
area it is assumed that an increased pressure is required t<> keep 
up elimination. This view has had very wide acceptance from 
clinicians who believed that a fall of pressure meant diminished 
urine and often led to uremia, and who therefore regarded the 
hypertension as compensatory and necessary. Experimental evi- 
dence, on the other hand, in a negative way indicates thai a) 
increased renal resistance is not the cause of h\ pertension; (6) that 
the latter does not cause an increased blood How through the 
kidneys; (c) that hypertension is not accountable for the polyuria. 

The results of experimentation, however, cannot in the presenl 
state of our knowledge be accepted as equivalenl to what occurs 
in human disease, because the entire problem is extremely complex, 
and because the syndrome which constitutes chronic interstitial 
nephritis has not yet been produced experimentally. 

Clinical Phenomena. — The rise of pressure which occurs in chronic 
interstitial nephritis is generally regarded as a compensatory 
effect. A certain amount of kidney substance lias been destroyed, 
but renal elimination must be maintained at any cost, and the 
cost is always a high one. More blood must pass through the 
renal vessels in a given time, and this Nature accomplishes by raising 
the blood-pressure in the renal arteries, which entails an elevation 
of the general systemic pressure. The latter greatly increases vas- 
cular wear and tear and, when the heart is capable of it, brings 
about a cardiac — chiefly left ventricular — hypertrophy. 

Lawrence, 2 who has reviewed this question, finds, however, that 
clinical reports are by no means unanimous in declaring hypertension 

1 Erlanger and Hooker: Johns Hopkins Hosp. Rep., 1904, xii, 145. Hooker: Am. 
Jour. Physiol., 1910, xxxvii, 24. 

2 The Relation of Hypertension to Urinary Excretion, Am. Jour. Med. Sc, Sep- 
tember, 1912, p. 330. 



294 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

to be compensatory and protective, and quotes numerous investi- 
gators to the effect that a lowering of pressure is coincident with 
symptomatic improvement. Lawrence's own studies show that there 
is no definite relation between changes in either the systolic or the 
diastolic pressure per se and alterations in urinary secretion, but 
that when an increased pulse-pressure results from a diastolic fall 
the urinary secretion is augmented. This occurred in only half 
of the cases in which the increased pulse-pressure was due to a 
systolic rise. Thus "an increase in the caliber of the vascular system 
seems to l»e more efficient in promoting diuresis than does increased 
pressure in the aorta and its great branches." 

It is the maximum pressure which is chiefly affected in nephritic 
hypertension; the minimum pressure lags behind, thus affording 
a larger amplitude. 1 In nephritic hypertension both the minute 
volume and the systolic output remain practically unchanged (Berg- 
mann and Plesch); indeed, they may even be subnormal in spite 
of the increased systolic and diastolic pressures. Nor is the rate 
of flow increased. Even pressures of 200 mm. may be accompanied 
by only a normal rate of flow, while a fall of pressure may actually 
mean an increased rate (Stewart). As a rule the blood-pressure 
increases gradually over a period of years, the individual appearing 
in perfect health, and is discovered perhaps accidentally while the 
patient consults the physician for some other ailment, or it may be 
that a palpitation of the heart, fulness of the head, gastro-intestinal 
disturbances, or dyspnea on exertion cause him to seek medical 
advice. Hypertension generally manifests itself symptomatically 
between fifty and sixty years of age. But high blood-pressure 
sometimes appears very early in cases of acute nephritis. Butter- 
mann in one case observed a rise of 50 mm. within forty-eight hours 
of the onset of albuminuria. 

Lee- found renal lesions in 71 per cent, of his autopsied cases 
of hypertension, and of these in 72 per cent, the lesion was atrophic. 
Arteriosclerosis was present in f> ( .) per cent., but in only 1 case 
could all other hypertensive factors be eliminated. Among the 
1.") cases in which no renal disease was found, 7 presented cerebral 
lesions. No patient without cither nephritis <>r arteriosclerosis showed 
a bloodrpressure of over 200 mm., mid nil who had a pressure constantly 
or repeatedly above this figure hud some rami lesion. 

Essentially similar results were observed among 150 cases at the 

i Musaer, •'• H., Jr.: The Relation <>f Ilit:h Systolic to Diastolic Pressure, Arch, 
1 diagnosis, July, I'M 1. 

Pathological Findings in Bypertension, Jour. Am. Med. Assn.. l'Ul.hii, 117!». 



\ EPHRITIC HYPERTENSION 295 

Heidelberg clinic, 1 as well as among .V><) cases studied by 
Fischer. 2 

Elevation of blood-pressure occurs chiefly in the atrophic kidney 
when the damage is mainlj glomerular. It occurs experimentally 
in uranium nephritis, and in such cases cardiac hypertrophy has 
been reported. 3 It may occur in exceptional cases of parenchj matous 
nephritis, hydronephrosis, etc., in explanation of which fact we 
have only to remember thai the pathological renal changes are 
often complex, and the lesions rarely limited exclusively to either 
the epithelial or endothelial structures. 

The phenolsulphonephthalein index tends to vary inversely with 
the average systolic, and especially the diastolic pressure, whereas 
the blood-urea nitrogen usually varies directly with the average 
blood-pressure. 1 

A high blood-nitrogen (70 to 120 mg., per 100 c.c), is often 
encountered in nephritic hypertension, but in the primary arterio- 
sclerotic cases normal readings are generally found. 

The feeding of protein bears a direct relation to the amount 
of nitrogen retention in the blood of nephritics, especially in inter- 
stitial nephritis associated with hypertension. This does not occur 
in passive congestion. Nitrogen retention is often associated with 
a low phthalein output and increased blood-pressure. 5 

The relationship between the nitrogen content of the blood and 
the degree of blood-pressure is, however, nol constant, although 
patients with a high index arc more subjeel to edema, nausea, 
vomiting and uremia.'"' 

Hyperglycemia of a slight degree was found by Hopkins 7 in many 
high-pressure nephritics, often in association with a low phthalein 
output. There is, however, no definite relation between the degree 
of hyperglycemia and that of hypertension. Most of the cases of 
nephritis without high blood-pressure have a normal amount of 
sugar in the blood. Venous blood-pressure is not increased in neph- 
ritis until cardiac insufficiency begins. 

1 Schonthaler: Bericht ueber in den letzten 4 Jahren an der Heidelberger Medi- 
zinischen Klinik beobachteten Hypertonien, Dissertation, Heidelberg, 1912, p. 39. 

2 Fischer, J. : Relations between Permanently High Blood-pressure and Kidney 
Disease, Deutsch. Arch. f. klin. Med., 1913, cix, Nos. 5-6. 

3 Siegel, W.: Ueber experimentale nephritis, Kongr. f. inn. Med., 1907, xxiv, 217. 
4 Cadbury, W. W.: Studies in Blood-pressure, Arch. Int. Med., 1916, xviii. 317. 

6 Hopkins, A. H., and Jonas L.: Studies in Renal Functions with Special Refer- 
ence to Non-protein Nitrogen and Sugar Concentration in the Blood, Phenolsulphone- 
phthalein Elimination and Blood-pressure, Arch. Int. Med., 1915, xv, 964. 

6 Seymour, M. : The Effect of Nitrogenous Waste Products in the Blood in Chronic 
Interstitial Nephritis, Boston Med. and Surg. Jour., 1913, clxix, 795. 

7 The Concentration of Blood Sugar in Health and Disease as Determined by 
Bang's Micromethod, Am. Jour. Med. Sc, 1915, cxlix, 254. 



296 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

Sodium Chloride Metabolism and Blood-pressure. — The elimination 
of sodium chloride from the diet of dropsical nephritics is sometimes 

attended by a marked increase of the urinary output. This sub- 
stance is often eliminated with difficulty and its retention in the 
tissues favors the retention of fluid. The effect of sodium chloride 
on blood-pressure is also a variable one. In some cases the institu- 
tion of a salt-free diet will definitely lower blood-pressure while 
chlorinization will produce an increase in pressure perhaps associated 
with general fluid retention and edema of the lungs. 1 Indeed it 
has been claimed that hypotensive properties of different medicinal 
substances owe their effects directly to their influence on the 
urinary chloride elimination.'- This view has been strenuously 
opposed by most investigators. Brodzki 3 was unable to produce 
a rise of pressure in nephritic cases by the administration of sodium 
chloride or meat extracts. (See page 248.) 

Blood-pressure and Urinary Secretion. — The relation between 
blood-pressure and urinary secretion is complex and not altogether 
understood. It has been established, however, that a certain 
minimum as well as intermittent pressure is essential to secretion, 
but above the said minimum pressure the rate of flow is much 
more important than the actual height of pressure. The effect of 
combined pressure upon the glomerular structure has been described 
by J. McCrae as follows: 

The capillary coil which we call the glomerulus has a large 
afferent vessel in which blood-pressure is high, and a small efferent 
vessel in which it is low. The glomerulus is therefore much more 
subject to wear and tear due to increased arterial pressure than 
are the tubular capillaries. "The kidney thus resembles a com- 
pound engine, in that most, if not all, the blood goes to the high- 
pressure cylinder, thence much of it goes to the low-pressure 
tubular capillaries, just as the stream, deprived of much of its 
expansive force, goes to the low-pressure cylinder; in all this the 
mechanical advantage is evident." (J. McCrae.) When, however, 
the glomeruli have as a result of incessant wear and tear, undergone 
hyaline degeneration, the high pressure is transferred to the tubules 
which stand this abnormal strain badly, and may rapidly become 
functionally insufficient. 

1 Ldwenstein: Ueber Bozichung zw. Kochsalzenthalt u. Blutdruck bie Nieren- 
kranken, Archiv f. exp. Path., 1907, lvii, 137. 

Elenea i. A.: Rapports de la Chlorure urinaire avec l'bypertension arterielle, etc., 
'I be e de Lyon, L909. 

per. Unterauch. u. d. Verhalten i!. Blutdrucks u. d. Einflua <ln- Nahrung auf 
denselben f. chroniacher Nephritis, Deutach. Arch. f. klin. Med., May, 1908. 



NEPHRITIC HYPERTENSIOh 297 

Experimentally it has been shown that the amount of urine 
excreted varies directly with the magnitude of the pulse-pressure. 
Exceptionally sudden vascular pressure changes ha \ e an augmenting 
influence. The chloride, urea and total nitrogen elimination gener- 
ally vary with the pulse-pressure. Reasoning from the foregoing 
facts, a drug which will increase pulse-pressure without markedly 
lowering the general blood-pressure or undulj constricting the 
renal arterioles, should he a good diuretic. 1 >i.uitalis and st rophan- 
thus fulfil these requirements and their diuretic effect appears to 
be Am- directly to their effed on pulse-pressure (Gesell . 

In disease the relation between urinarj outpul and blood-pressure 
is not constant. This nia\ be due to nervous influence by virtue 
of which the supply of renal blood does not stand in proportion 
to the general blood-pressure. It cannot be due to exacerbations 
of local inflammation because, as Herringham 2 declares, the "ap- 
parent discrepancy alters from day to day in so inconstant a manner 
that no fresh access of inflammation can explain it, and in the 
second place we should expect, if that explanation were true, that the 
albumin should vary with the inflammation. A fresh attack would 
probably result in an increase of the albumin. Butnosucb variation 
takes place constantly in the albumin. The decrease "I' urine 
is not always accompanied by an increase in the proportion of 
albumin." 

As a general rule, however, low-pressure cases excrete less urine 
than high-pressure cases, and the most satisfactory diuretics do 
not have a depressor action. The complexity of the problem and 
the likelihood that numerous factors have a variable effect on 
blood-pressure is shown by the following observations : 

"In a case of nephritis with albuminuria and persistently high 
arterial pressure studied by Stewart 3 the pressure was reduced by 
forced breathing. This effect was in part due to an increased 
elimination of carbon dioxide by the lungs and to mechanical inter- 
ference with the circulation. The administration of large doses of 
sodium bicarbonate was also associated with a marked fall of 
pressure. In another case the withdrawal of cerebrospinal fluid 
reduced the arterial pressure apparently by lowering intracranial 
pressure. No pressor substance could be demonstrated in the 
cerebrospinal fluid." 

1 The Relation of Pulse-pressure to Renal Secretion, Amer. Jour. Physiol., 1913, 
xxxii, 71. 

2 Kidney Diseases, London, 1912, p. 220. 

3 So-called Biological Tests for Adrenalin in Blood, with some Observations on 
Arterial Hypertonus, Jour. Exp. Med., 1911, xiv, 4. 



298 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

The Complications of Hypertension. — I. Uremia. — Chronic uremia 
is associated with high, acute uremia with very high, blood-pressure. 
The latter is sufficiently marked to be of great diagnostic value. 
The increment in pressure depends largely on the height of the 
preceding average pressure. When this lias been low, increases of 
100 per cent, are not unusual. 

The cause of these sudden increments of tension is not and 
cannot be known until the causes of hypertension in nephritis and 
the nature of uremia have been elucidated, but the hypothesis that 
many of the uremic symptoms are the direct result of abnormal 
local pressure relations is extremely plausible. 

The symptoms of uremia are well known and require no special 
consideration. All of the transient nervous phenomena described 
under Cerebral Vascular Crises (see page 2G9) may result from 
uremia. Vascular spasm may be the etiological factor in either case. 

II. Paroxysmal Dyspnea. — Paroxysmal attacks of increased ten- 
sion and dyspnea are not uncommon in arteriosclerotic subjects, 
especially with renal involvement. It is quite likely that these 
phenomena are due to irritation or disease of the depressor nerve 
in the aorta, hence they are encountered especially in cases of 
syphilitic aortitis. Bittorf 1 has reported degeneration of the depressor 
nerve in two patients with aortic sclerosis (aged forty-three and 
fifty-six years) associated with hypertension and cardiac hyper- 
trophy. 

"Having still more important bearing on this subject are some 
old experiments of Francois Frank 2 on aortic reflexes. By irritat- 
ing the inner surface of the aorta of dogs he was able to produce 
quite constantly certain respiratory phenomena. These consisted 
of three types: (1) Sudden apnea with the respiratory muscles in 
spasm either during the inspiratory or expiratory phase, or apnea 
with general inhibition of all respiratory movements; (2) tachypnea 
without severe constitutional symptoms, and (3) a slow dyspnea 
of severe and grave form. The cause of this dyspnea he showed 
quite plainly was spasm of the bronchial musculature. lie believed, 
too, that there was coincident contraction of the pulmonary artery. 
Associated with this type of dyspnea was a contraction of the 
peripheral vessels and rise of blood-pressure. Occasionally a spasm 
of the laryngeal muscles occurred. In other eases he was able to 
produce all the signs of aortic insufficiency (the capillary and 
collapsing pulse) save a diastolic murmur through irritation of 
the root of the aorta and without injury to the sigmoid valves. 

1 Deutsch. med. Wchnschr., 1910, No. 46. 
\rrh. ,lc Physiol., L890, series ">, ii, 508 and 547; Jour, de I'anat., 1N77, xiii, 546. 



NEPHRITIC HYPERTENSIOh 299 

Stewart 1 bas observed this last phenomenon and con iders it as a 
reflex from the root of the aorta, and in some experiments in which 
aortic insufficiency was performed on dogs I have repeatedly 
confirmed this observation. Thai Frank's respiratory phenomena 
have not been noted since is almosl certainlj due to the method of 
experimentation, for in Stewart's experiment, and in those which 
others have performed, full ether anesthesia or artificial respiration 
was employed. 

" It is thus evident that disturbing reflexes may be set up experi- 
mentally in animals by irritation of I he rootofthe aorta, and there 
is no reason to suppose t hat the same thing should tiol be true for 
man. The dyspnea caused by bronchiospasm, and the contraction 
of the peripheral arteries producing heightened blood-pressure in 
the experimental animal is a close reproduction of the paroxysmal 
dyspnea as it occurs in syphilitic aortitis, and it seems quite justi- 
fiable to suggest that the two conditions are the same. It would 
be difficult to explain the increase in blood-pressure which occurs 
during these attacks in man on the presence of pain or of cyanosis, 
for pain is frequently absent and dyspnea may continue for some 
time (fifteen to thirty minutes) after the sudden drop in blood- 
pressure which comes with the relict' of acute symptoms. Our 
observations therefore seem to lend strong supporl to the idea 
that these symptoms are dependent on a reflex generated at the 
root of the aorta by the syphilitic inflammatory process. 2 The 
attacks have been found to consist of three phases: (1) A very 
high systolic and diastolic pressure 210 190; (2) falling pressures 
in which the diastolic may remain disproportionately high a had 
sign); (3) a gradual return to the normal." 

Paroxysmal dyspnea may also occur when the cerebrospinal 
pressure becomes too high. Such attacks may be associated with cere- 
bral symptoms — headache, vomiting, vertigo, and with subjective 
oppression and respiratory acceleration, but without preexisting 
asthmatic symptoms. It has been suggested that although certain 
forms of non-cyanotic dyspnea frequently described as "renal" 
or "cardiac" are associated with high blood-pressure, they are 
basically due to renal defects and are directly dependent upon an 
acid intoxication. 4 Peabody's 5 studies showed that when acidosis, 

1 Archiv. Int. Med., 1908, i, 102. 
2 Longcope: Arch. Int. Med., January, 1913. 

3 Amblard, L. A. : La Tension Arterielle dans l'oedem aigu du Poumon, Presso 
medicale, 1911, xix, 657. 

4 Lewis, Ryffel, Wolf, Cotton, and Barcroft: Observations Relating to Dyspnea 
in Cardiac and Renal Patients, 1913, Heart, v, 45. 

5 The Effect of Carbon Dioxide in the Inspired Air on Patients with Cardiac 
Disease, Arch. Int. Med., 1915, xvi, 846. 



300 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

as indicated by the alveolar carbon dioxide tension, occurs in cardiac 
and cardiorenal disease, it is associated with an increased stimula- 
bility to carbon dioxide in the inspired air. In patients of this class 
dyspnea occurs more readily than in normal subjects or in patients 
without acidosis. lie was led to conclude that while acidosis is 
probably not the only factor in cardiorenal dyspnea it may play a 
considerable role. The acidosis of nephritics is mainly due to acid 
phosphates and not as in case of diabetics to ketones. 1 

A lowering of the blood-pressure often brings relief in attacks 
of paroxysmal dyspnea. If acidosis is a factor the administration 
of sodium bicarbonate should be tried. 

When dyspnea (asphyxia) is the cause of the hypertension, 
bleeding, digitalis and general measures are indicated. In the 
( heyne-Stokes type of breathing, lumbar puncture, which relieves 
cerebrospinal pressure, is in order, although it has not much effect 
upon the general pressure. Morphin is useful in either type. 2 

III. Cheyne-Stokes Respiration. — Cheyne-Stokes breathing is fre- 
quently encountered in association with arterial hypertension. 
This symptom when occurring in association with experimentally 
increased intracranial tension has been shown by Gushing 3 to be 
accompanied by high pressure during hypcrpnea and low pressure 
during apnea. The importance of this fact from a clinical stand- 
point in order to differentiate between Cheyne-Stokes respiration 
with and without increased intracranial pressure was demonstrated 
by Eyster; 4 the findings of the latter were corroborated by Pollock, 5 
who explains the exact mechanism of the symptoms as follows: 

"The intracranial tension being higher than the general blood- 
pressure, cerebral anemia exists and apnea is present. The vaso- 
motor centres are automatically stimulated to raise the general 
blood-pressure in an effort to produce an equilibrium between it 
and the intracranial tension. As the general blood-pressure rises, 
respiratory movements recommence; at their height the vasomotor 
centres are no longer stimulated, the general blood-pressure again 
falls, and the respiratory movements diminish and finally cease." 

Hyperpnea is associated with increased amplitude of the apex 
beat, and the pulse rate increases with the rise of blood-pressure. 
Arrhythmia and prolongation of the a-c interval may also occur. 

i Howland, J., and Marriott, W. M.: Jour. Dis. Child., 1916, xi, 309. 
'Pal, •'•: Paroxysmale Bochspannungsdyspnea, Vienna, 1907. 

Am. Jour. Med. Sc, 1902, exxiv, 375; 1903, exxv, 1017. 
• Johna Hopkins IIosp. Bull., L906, xvii, 296. 
1 Blood-pressure in Cheyne-StokeB Respiration, Arch. Int. Med., 1912, ix, 406. 



NEPHUlTie HYPERTENSION 301 

Symptomatic relief often follows lumbar puncture, which tem- 
porarily reduces intracranial tension. 

From Eyster's investigations it would seem that the stimula- 
bility of the respiratory centre is at a permanently low level, which 
requires an abnormally intense stimulus to produce a response, 
the stimulus being supplied by the toxic products which have accu- 
mulated in the blood through apnea and low pressure. The admin- 
istration of CO2 toward the end of the hyperpneic period has in 
one instance prevented the recurrence of the apneic periods. 1 

IV. Acute Pulmonary Edema. Pulmonarj edema may occur 
in patients with chronic vascular hypertension. Attacks are pre- 
ceded by a rise of both systolic and diastolic pressures. During 
the attack the maximum pressure, which has been very high 240 
to 280 mm.), falls greatly, the minimum slightly. At such times 
venesection, although often beneficial, exert- bu1 little effed on the 
pressure. After the attack, in cases which recover, pressure rises 
gradually to the normal. These symptoms, as was first shown 
by Welch and ( 'ohnheim,-' find their explanation in the fact that 
a temporary left ventricular failure, while causing a fall in the 
systemic circulation, produces a great stasis rise in the pulmonary 
vessels which the right ventricle is no longer able to overcome, 
and which either in isolation or in association with toxins leads to 
serious oozing or vascular rupture into the pulmonary parenchyma. 
Experimentally, epinephrin may produce pulmonarj edema through 
vascular degeneration, alveolar inflammation, and increase of 
pressure. It may also be produced by clamping the aorta or com- 
pressing the left ventricle. The increased pressure in the left 
ventricle is transmitted backward to the pulmonary vessels, thus 
raising pressure in the pulmonary artery. This, if of sufficient 
degree tends to cause a serous transudation into the alveoli. A 
similar effect may, however, arise from marked passive dilatation 
of the pulmonary capillaries. Heart failure results when the gaseous 
metabolism which is diminished in these cases fails to supply the 
required quota of contractile energy. 3 The primary disturbance 
therefore seems to be some influence on the nervous system which 
interferes with the normal regulation of the correlated vascular 
tension, heart action, and respiration in the case of an already 

1 Observations on Two Cases of Cheyne-Stokes Respiration, Jour. Physiol., 1906, 
xxxiv, 6. 

2 Gesammte Abhandl., Berlin, 1885, p. 594. 

3 Matsuoka, Y. : Contribution to the Pathology of Obstructive Edema of the 
Lung, Based upon Observations with the Starling Heart-lung Preparation, Jour. 
Path, and Bact., 1915, xx, 53. 



302 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

diseased heart. 1 It has been suggested that attacks of pulmonary 
edema in nephritics arc the result of an effort on the part of the 
id to rid itself of urea and chlorides.' Among 405 cases of 
pulmonary edema postmortem, Coplin found renal lesions in 333. 
An early and marked fall of pressure may result from cardiac 
exhaustion. 

Prognosis. Chronic arterial hypertension is a serious condition 
which generally spells chronic interstitial nephritis. The degree 
of hypertension hears no constant relation to the severity of the 
nephritis as determined by the routine urine examination, the 
phthalein elimination or the amount of nitrogen retention. The 
mildesl cases may show the highest pressure. 

The absence of hypertension in a ease which presents the other 
clinical evidences of chronic interstitial nephritis suggests the exist- 
ence of a tuberculous, syphilitic or amyloid lesion of the kidney. 
When associated with severe cardiac symptoms and retinal hemor- 
rhages a lethal termination may be expected within a few years. 
The teaching was formerly current that nephritic retinal hemor- 
rhages were invariably followed by death within a period ranging 
from ^i.\ months to two years. While this is doubtless true in the 
glomerulonephritic group, especially if hemorrhages are severe and 
recurrent, yet in individuals of the arteriosclerotic type, particularly 
those who can and will modify their manner of life, there can be 
no question that such a prognosis is unnecessarily austere. Many 
cases of retinal hemorrhages are not seen by the ophthalmologist 
in their early stages. Plenty of cases are on record in which patients 
have lived ten years or more after the onset of nephritic retinal 
hemorrhages. It is a common observation that patients having a 
pressure ranging around ISO mm. (systolic) and 110 mm. (diastolic) 
without marked urinary findings, or of ocular or cardiac symptoms, 
may live for many years. Strauss 3 has reported the case of a patient 
who lived five years with a systolic pressure ranging between 260 and 
270 mm. Ilg. (See page 136.) Hypertensive cases are apt to have 
exacerbations of pressure (200 mm. and over) associated with more 
or less troublesome symptoms— insomnia, nervousness, irritability, 
weakness, fatigue, inability to concentrate attention, mental depres- 
sion, dyspnea, precordial oppression, etc. — which will under appro- 

tnblard, A.: Presse medicale, August 12,1012. Petren: Bert, klin. Wchnsrhr., 
I December -7, vol. xlvi. 

1 Lesieur, Froment, and Etochaix: Oedemea aigua dn poumon. Comparison du 
taui ilc I'uree el de chloruree dans I'- serum sanguin et dans 1'expectoration, Soc. 
med. dea B6p., Paris, November 19, L909. 
Deutscb, med. \\ chnschr., L915, xli, No. Id. 



\ EPHRITIC II) PERTENSIOh 303 

priate treatment subside. Such cases are regarded as bad insurance 
risks, and justly so, and yel with an intelligent comprehen ion of 
their condition and a willingness to cm-tail the expenditure of 
energy, they may lead lives of usefulness and comparative comfori 
for many years. These statements are borne out by Pae ler' 
graduated nephrectomy experiments. The prognosis therefore 
often hinges quite as much <>n the individual as on the disease. 
The occurrence <>f well-marked edema in hypertensive cases is more 
serious than in eases of valvular disease. The following rules, as 
laid down by Lichty, 2 indicate the general lines upon which a prog- 
nosis may be based: 

"1. Where hypertension exists with bu1 little or no recognizable 
disturbed function of other organs the outlook is most favorable. 
(2) Where it is associated with marked disturbance of any one 
other organ alone it is more serious. (3) Where it is associated with 
great defect of several other organs, such as kidney insufficiency, 
cardiac insufficiency, cirrhosis of the liver, and lesions of the gastro- 
intestinal tract, the prognosis is most serious. (4) When the hyper- 
tension is associated with sympt - and physical signs which 

disappear after a more or less active and prolonged treatment which, 
however, fails to lower the tension, a favorable prognosis is not 
unwarranted. Such cases are rather frequent, and I believe it is 
just as unreasonable to take an unfavorable view of them as it is 
to predict a speedy fatality in all cases of pulmonary tuberculosis 
where the bacilli are found in the sputum. (5) When the ten. inn 
is found in connection with changes in organs producing such 
extreme symptoms as dropsy, ascites, cyanosis, and orthopnea, 
and when these symptoms cannot be relieved, whether the tension 
is modified or not modified by heroic treatment covering five to 
eight weeks, then defeat is sure." 

As to the cause of death in hypertension, this may result from 
apoplexy, uremia, angina pectoris, broken cardiac and vascular 
compensation, or from intercurrent disease. Among 565 cases of 
renal disease at St. Bartholomew's Hospital 209 died from renal 
disease as follows: 

Sudden death without any other sufficient cause 9 

From uremia 28 

From cerebral hemorrhage 82 

From cardiac failure 90 

209 

1 Samml. klin. Vortrage, No. 408. 

2 Hypertension : A Report of Cases under Prolonged Observation, and a Protest 
Against Some Ideas, Am. Jour. Med. Sc, May, 1913. 



304 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

The following tables are taken from Janeway's article based on 
a study of 100 cases -with a blood-pressure of or above 170 nun. Hg. 

The Age of the Patients. 
Below 20 years 2 cases, about 2 per cent. 



20 i,i2!) " () 

30 to 39 " 3 

40 to 49 " 24 

50 to 59 " 39 

(>n to 68 " 32 

70 and over 11 



The Duration of the Illness in Relation to the Causes of Death. 









Duration. 








Average. 


Longest. 


Shortest. 


( auscs of death. 


( &8e8. 


■"i cars. 


Months. 


Years. 


Years. Mont 


< lardiac insufficiency 


. 20 


3 


10 


10 


4 


Acute uremia 


14 


3 




8 


5 


( Ihronic uremia . 


. 21 


3 


1 


7 


4 


Cerebral apoplexy 


. 14 


4 


6 


11 


11 


Angina pectoris . 


3 


4 


3 


6 


3 6 


Acute edema of lungs 


4 


3 




4 


1 8 



The Immediate Cause of Death. 

Gradual cardiac insufficiency 29 

Uremic convulsions or sudden coma 15 

Chronic uremia 20 

Uremic psychosis 1 

Cerebral apoplexy 14 

Acute edema of the lungs 4 

Angina pectoris 3 

Sudden death (unclassified) 4 

Progressive anemia 2 

Acute pneumonia 1 

Unrelated diseases 4 

100 

Stone 1 has called attention to the fact that the cardiovascular 
type of hypertension can be differentiated from the nephritic, or as 
he prefers to designate it, the cerebral type, by the pulse-pressure 
and the cardiac l<><nl (see page 275). Thus in arterial hypertension 
associated with valvular or myocardial lesions, the diastolic pressure 
is persistently lower than in the cerebral type. Hence with an 
equal systolic pressure the overload is increased — in 24 patients 
to an average of 46 per cent. Such a differentiation has a good 
deal more than an academic importance because both prognosis, 
therapy and mode of death vary very distinctly in the two types. 

'The Differentiation <<f Cerebral and Cardiac Types of Byperarterial Tension 
in Vascular Disease, Arch. [nt. Med., 1915, xvi, 775. 



NEPHRITIC HYPERTENSIOb 



: !l 15 



Hypertensive disease as seen in hospitals presents a very different 
picture from that seen in private practice. In the former instance 
we see chiefly the terminal stages. Since the alleviation of mp- 
toms as well as the prolongation of life depends mainlj upon an 
early recognition of the condition, it is important to know tin- early 
symptoms from which patients have suffered. These are shown 
in the following table from Janeway's article. 1 



Tin: Relation of Prominent Barli Symptoms with High Bl i > 

I.. Causes oj Death. 



Symptoms, 


i - of death, 




a . 

O c. 
03_O 

3 % 
G 


P 


a 


1 

a 
■a 
'3 
5 

a 

< 


a 

| 

- 


r. 

'§ 

I 


■- 
-r 
W 


— 5 

— — 


§1 


sa 

1 

- 


g I 
-= - 
7 a 
^ = 
a >■ 


— 
y. 


24 


13 


i 


r, 


7 


s 


1 


l 


L' 


2 


1 


Gradual cardiac insuffi- 
ciency 


29 


7 


2 





l 





7 


2 


l 


2 


3 


3 


Uremic convulsions or 
sudden coma 


15 


5 


1 


2 


3 





11 


8 


5 


-1 


.", 


1 


< Gradual uremia 


20 


6 


2 





2 


2 


2 


2 


1 


4 





■1 


::1 apoplexy or its 
results 


14 


1 


1 





2 














n 








Angina pectoris 


3 


2 


2 


1 


1 


1 


1 











1 


1 


Edema of the lungs . 


4 


3 


3 





1 


1 


3 


2 





1 


3 





Other causes .... 


15 


48 


24 


4 


15 


11 


32 


15 


8 


13 


14 


,.. 




100 



It is evident from the foregoing tables that cardiovascular failure 
is the commonest cause of death, while uremia and apoplexy are 
frequent, and angina pectoris is relatively rare. Early ocular 
changes are often followed by uremic death. A certain number 
of cases die as the result of a progressive anemia which has its 
basis in the renal lesion, and a small number from acute pulmonary 
edema. 

Janeway's careful analysis of cases of hypertensive cardio- 
vascular disease showed that the average duration of life in these 
cases after the onset of hypertension was four years for men and 
five for women. During the first five years one-half the cases 
died, one-quarter lived between five and ten years, and the remainder 
over ten years. He further found that definite prognostic con- 



1 A Clinical Study of Hypertensive Cardiovascular Disease, Arch. Int. Med. 
xii, 755. 
20 



306 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

elusions, based upon the actual height of the pressure found, were 
unwarranted. 

Certain conclusions may generally he drawn as to the ultimate 
manner of death from the history and the physical signs. Thus 
the early onset and predominance of dyspnea or other symptoms 
i if cardiac weakness indicates "a more than 50 per cent, probability 
of an eventual death by cardiac insufficiency." The occurrence 
of anginoid pain may he similarly interpreted, although only one- 
third of these eases actually die in a paroxysm of angina pectoris. 
In contrast to these cases patients with polyuria, especially if 
nocturnal, and those with headaches present on waking and gradu- 
ally disappearing, will in about 50 per cent, of instances die of 
uremia. Progressive or marked loss of weight is a had symptom 
(Janeway). A disproportionately high diastolic pressure (120-150) 
is more serious than a very high systolic pressure, and appears to 
increase the likelihood of a uremic or apoplectic death. A high 
systolic pressure with only a moderate increase in the diastolic 
tension points toward a prohable death from cardiac decompensation. 

Total number of As a first 
Symptoms. patients. symptom in. 

Dyspnea (on exertion and paroxysmal) .... 20 6 

Anginoid pain 16 6 

Edema of lungs 2 

Palpitation 13 8 

Edema of the legs 8 1 

General edema 1 1 

Polyuria 6 2 

Retention of urine 2 2 

Headache 12 1 

Vertigo 9 3 

Hemiplegic attacks 5 1 

Transient coma 1 1 

Uremic convulsion 1 

Drowsiness 1 

Visual disturbances 1 

Pains (mainly neuralgia) 8 3 

Fatigue (physical and mental) 6 1 

Hemorrhages 3 

Loss of flesh 2 

igrene of extremities . . 1 1 

Intermittent claudication 4 1 

Cough 1 

Diabetes 10 6 

Albumin and casta (accidental discovery) ... 3 3 

Cardiac disturbance (accidental discovery) . . 2 2 

1 1 ii-li M "nd-pressure (accidental discovery) . . 1 1 

Acute Nephritis. Even in children acute nephritis often produces 
a marked elevation of blood-pressure which is of distinct diagnostic 



\/ PHRITIC in PERI ENSIOh 307 

value, but the rise of pressure dues not always occur. The pre ore 
may van according as the glomeruli or tubules arc chiefly involved. 

hi some cases the amounl of 1)1 1 or albumin in the urine seem to 

bear a relation to the heighl of the pressure. The mean average 
pressure is not so high as in chronic nephritis, and during the beighl 
of some infectious fevers the blood-pressure rise entailed by the 
nephritis may be more or less counter-balanced bj the h\ potensive 
effeel of the febrile toxemia. Cardiac h\ pen rophj maj be noticeable 
in children and young adults four weeks .after the onsel of scarlatinal 
nephritis. 1 Rolleston found a temporary rise of pressure in 12 out 
of 33 such eases. 

Recent observations upon several hundred soldiers returned 
from the war /.one on account of acute nephritis showed a striking 
diurnal variation of pressure sometimes amounting to 60 mm. Hg. 
In the early stages the pressure changes were irregular, hut later, 
morning remissions gave place to evening increments, producing 
when charted a "staircase" form. In some cases a period of sub- 
normal readings were obtained w ith a subsequenl rise to the normal. 

In the majority, the pressure became normal as albuminuria dis- 
appeared, although in some instances the patients were scut home 
with hypertension. Uremia was generally associated with high, 
sometimes very high (200 mm. Ilg.) readings. Marked nocturnal 
rises were not infrequently associated with headache and par- 
oxysmal dyspnea. 2 

Mercurial Poisoning.- Poisoning with the mercurial salt- pro- 
duces renal necrosis associated with anuria. Janeway and M Tiller 
have reported cases of bichloride poisoning with increased blood- 
pressure (170 mm.) until the terminal fall occurred. 3 

Polycythemia. — Arterial hypertension occurs in some cases of 
polycythemia; indeed, a special type of this disease is often alluded 
to as polycythemia hypertonica. The fact that increased blood- 
pressure is not a constant finding shows that the origin of this 
symptom cannot lie in increased hemic viscosity, which is present 
in all cases, and which is doubtless often counter-balanced by 
reflex vasodilatation. Ordinary hypertension has no direct or 
constant relation to the erythrocyte count. 4 

1 Friedlander: Arch. f. Physiol., 18S1, p. 16S. 

2 Abercrombie, R. G. : Systolic Pressure in Acute Nephritis, British Med. Jour., 
1916, June 23, I, No. 2895. 

3 Janeway, T. C: Nephritic Hypertension, Am. Jour. Med. Sc, Ma5', 1913, 651. 
Muller, F.: Quoted by C. Thorel, Path. d. Kreislaufsorgane, Ergebn. d. allg. 
Pathol, u. path. Anat., 1910, xiv, 133. 

4 Moller: Deutsch. med. Wchnschr., October 29, 1908, xxxiv. 



308 ARTERIAL HYPERTENSIVE CARDIOVASCULAR DISEASE 

In Lucas's 1 collection of 179 eases the blood-pressure was reported 
in 66 instances as follows: 

Blond-pressure, 145 to 170 23 

180 to 200 13 

" " 210, 235, 240, and 310 (one each) 4 

220 3 

200 2 

"The blood-pressure is usually above normal in eases showing no 
splenomegaly (Geisbock's polycythemia hypertonica)." Miinzer 
suggests that polycythemia may result from arteriosclerotic changes 
in the hemopoietic organs, which refiexly bring about an increased 
blood-pressure and increased functional activity. 

Thai the increased blood-pressure noted in some cases is not, as 
is sometimes stated, due to increased viscosity of the blood is shown 
by the following facts: (1) no definite relation has been shown to 
exist between increased viscosity and hypertension. (2) Hyper- 
tension bears no relation to the degree of polycythemia and upon the 
latter the hyperviscosity mainly depends. (3) Experiments 2 have 
shown that increased viscosity tends to diminish cardiac intake 
and hence should, if it had any effect, lower blood-pressure. 

Arterial Hypertension and Hemic Viscosity. — Martinet 3 has 
studied the pressure-viscosity relation in a large series of cases, 
and based upon this investigation classifies them as follows: 

1. Eusystolic type, in which the relation between maximum 
pressure and blood viscosity yields a quotient close to 4 (3.8 to 
L5). These cases even if the pressure is abnormal possess no 

serious renal nor cardiac lesion. 

2. Hypersystolic type, with a sphygmoviscometric index greater 
than 4.5, an increased tension with a lowered viscosity. These 
cases have sclerotic kidneys, left ventricular enlargement, polyuria, 
hydruria, and a tendency to vascular rupture. 

3. Hyposystolic type, index less than 3.5, low tension and high 
viscosity. Venous stasis: emphysema, tuberculosis, mitral lesions, 
cyanosis, dyspnea, enlargement of right heart. 

He believes that in the second type the hypertension begins 
as an increased viscosity (from overnutrition), which falls when 

the kidneys begin to fail and the bl 1 becomes more dilute, lie 

therefore distinguishes two classes of hypertension: 

i Erythremia or Polycythemia with Chronic Cyanosis and Splenomegaly, Arch. 
Int. Med., L912, x, 597. 

is, C. I-, and Ogarva, B.: Jour. Physiol., 1915, riix. 
Pressione arteriellcs et viscositr sanguine (circulation, nutrition, diurese), Paris 

■i-'. 



ARTERIAL HYPERTENSWh 309 

(a i simple hypertension i li\ pen i co it; 

(6) Cardiorenal hypertension (hypoviscosit; . and considers thai 
both prognosis and treatmenl are quite different in each case. 
Thus in two cases the iodides increased pressure, dropsy, and 
albuminuria, Class (6), while the iodides proved beneficial in Class 
(a). He further suggests thai much light may be thrown upon 
the action of certain drugs (purgatives, diuretic-' and other thera- 
peutic measures (hydrotherapy, etc.) bj a study of the sphygmo- 
viscosity index. 

Pellissier's 1 studies led bim to believe that in cardiac di ease 
and in gestational toxemia a fluctuating blood-pressure associated 
with an increased hemic viscosity is of very serious imporl and in 
pregnancy often an indication for immediate active treatment. 

1 Arch. Mens. d'Obstet. el de I Syn., 1915, Lv, No. 5. 



CHAPTER XIII. 

THE TREATMENT OF ARTERIAL HYPERTENSION. 

• Hypertension per se is no more of an indication for treatment, 
except along preventive lines, than is the presence of a heart 
murmur. Hypertension is one of Nature's methods of compensat- 
ing circulatory or visceral deficiency, and in the carrying out of 
her purpose she can fortunately not often he thwarted. Reduce 
the pressure in a case of Br'ght's disease by violent means, such as 
the nitrites, if you will. After a very brief space of time the pressure 
will rise to its former height. The direct reduction of blood-pressure 
by means of drugs or otherwise is a procedure which should only 
be undertaken after the most careful consideration of the case 
from all its aspects. We must never thoughtlessly or ruthlessly 
interfere with Nature's delicately balanced mechanism of com- 
pensation. Only in the face of impending circulatory failure or 
vascular rupture or temporary pain is direct treatment indicated. 
On the other hand, in arterial hypertension, as Langdon Brown 
has aptly put it, "the patient is living too close to the limits of 
his cardiac reserve," and often a very high pressure can be more 
or less reduced without producing any deleterious results and 
wiih marked symptomatic amelioration, to say nothing of the 
saving of cardiovascular wear and tear. Just how much pressure 
lowering is possible and desirable must be determined for each 
individual case, and in practically no instance is such an effect 
to be sought merely by the administration of drugs. Treatment 
is generally much more satisfactory and its effects more lasting 
in cases showing only moderately increased pressure. This has 
been well expressed by Brooks, in saying that hypertension is not 
pathological but is usually, if not always, physiological in import; 
thai it tends to prolong life rather than to shorten it, and that 
when its causes cannot be removed it should not be treated but 
maintained. 

The reduction of vascular hypertension relieves the heart of an 
immense amount of work entirely unnecessary work in cases in 
which the high arterial pressure results from the toxic factors 
attendant upon a faulty mode of living. 



DIRECT REDUCTION OF BLOOD-PRESSURE 311 

"The heart, beating at the rate of 70 times a minute, i. < ., 1200 
times an hour, 100,800 times daily, ami 36,792,000 times annually, 
would pump on an average 2^ ounces of Mood at each contraction, 
17."» ounces a minute, 6564 pounds an hour, or 1\ torn a day," 
which "is equivalent to lifting one ton L22 feel high." 1 

Since about 10 pounds of blood arc pumped by the heart per 
minute it is self-evident that an increase of pressure ranging be1 ween 
10 and 50 mm., not to mention higher figures, must call for the 
expenditure of an enormous amount of cardiac work. Further- 
more, the heart which is called upon to meel such demands is often 
already affected by arteriosclerotic changes. The wear and tear 
on the vascular system is of course a no less important factor. 
Dilatation of the aortic arch, even in aon-syphilitics under fiftj 
years of age is of frequent occurrence in cases of nephritic hyper- 
tension. 2 The entire hydrodynamic system is working under a 
continuous condition of forced draught. Brunton has suggested 
that hypertension does harm not only by interfering with tissue 
nutrition but also by hindering the vascular supply of the arteries 
themselves; the vasa vasorum being compressed between the 
intima and the adventitia of the arterial wall, whereas the alternate 
contraction and expansion which occurs in health, exercises an 
effect like massage which favors the nutritional How. 

The Direct Reduction of Blood-pressure. — Blood-pressure should 
very rarely be directly reduced by means of drugs or venesection 
except in case of emergency. The term emergency in this connection 
includes : 

1. Cases with or without excessively high pressure (200 mm. -f ) 
in which owing to the presence of symptoms such as vertigo, head- 
ache, numbness, tingling, loss of power, mental confusion or actual 
palsy, an apoplexy is feared. Cases of aortic aneurysm with 
symptoms of imminent suffocation. Also cases of acute pulmonary 
edema. Venesection is the method of choice. 

2. Cases with threatened or actual angina pectoris. Here the 
nitrites, especially nitrite of amyl, are useful. 

3. Cases with high pressures in which a cataract extraction is 
to be performed. Sodium nitrite or erythrol tetranitrate will lower 
blood-pressure and diminish the risk of intra-ocular hemorrhage. 

In addition to the foregoing types, Nicholson 3 has suggested the 

1 Pope, C: Month. Cyclop, and Med. Bull., January, 1910. 

2 Smith, W. H., and Kilgore, A. R. : Dilatation of the Arch of the Aorta in Chronic 
Nephritis with Hypertension, Am. Jour. Med. Sc, 1915, cxlix, 503. 

3 The Clinical Significance of Blood-pressure, Med. Record, March 20, 1915. 



312 TREATMENT OF ARTERIAL HYPERTENSION 

use of the nitrites in hypertension cases about to be anesthetized. 
This would, however, seem of questionable advisability owing to 
the dangei of increasing "shock" (see page 396). 

If general treatment does not reduce blood-pressure the kidneys 
are probably sufficiently sclerotic to require the excess of pressure. 
A pressure of 200 or over rarely returns to normal. A pressure 
which has stood as high as 200 for more than a very brief interval 
cannot he expected to fall much below 160-170. This may be 
considered a satisfactory attainment. Many cases after carrying 
a pressure of about 180 for several years gradually show a decline 
to 150 or lower owing to myocardial weakening. A fall below this 
point in long-standing cases does not offer a propitious outlook. 

There are often two factors concerned in the production of arterial 
hypertension: (1) A basic or essential factor, the point to which 
pressure must be raised to maintain metabolism, and (2) a super- 
added or toxic factor which results from faulty habits of life. It 
is the latter only which we are justified in treating. Ordinarily 
a pressure of 190 mm. or over is an absolute indication for entire 
cessation from work, and generally rest in bed, at least until the 
case has been carefully studied. 

The following history is illustrative of what may be accomplished 
in cases of hypertension: 

Mr. B., aged sixty-one years, high-strung, intellectual, always a 
hard worker, president of a large manufacturing company, presented 
himself in L908 complaining of fatigue, nocturnal micturition, head- 
aches and palpitation, loss of weight, and anginoid attacks. Blood- 
pressure: systolic, 200; diastolic, 120 mm. 

The arteries were very sclerotic, hard, and tense, the temporal 
vessels prominent, the eyes injected, the heart enlarged to the left 
wit 1 1 aortic accentuation, a systolic mitral murmur, and a redupli- 
cated first sound. Trine: trace of albumin with hyaline casts. 

He has intelligently cooperated in carrying out the treatment, 
which consisted in lessening his working hours, avoiding hurry 
and worry as much as possible, relegating all unessential work and 
needless telephone calls to others. Moderation in diet and rest in 
the recumbent posture late each afternoon. Occasional sweat 
baths, with spinal massage. 

In L917 he is comfortable, puts in a long day's work, but realizes 
his limitations and submits to them, lie plays golf actively and 
his pressure ranges between 165 and 185, the diastolic element 
between 85 and 95 nun. He belongs to the arteriosclerotic not the 
glomerulonephritic group. 



DIRECT REDVCTIOh OF BLOOD PRESSl M 313 

He occasionally bas hypertensive attacks brought on by undue 
strenuosity which yield to full doses of nitrites, purgation, rest in 
bed, and a milk diet, but, on the whole, Feels vastly better and 
accomplishes essentially as much as be did nine years ago. 

The treatment of nephritic hypertension is fraught with difficult ies 
and requires the best of judgment. High blood-pressure leads to 
cerebral hemorrhage and cardiovascular failure, but high pressure 

is compensating and necessary ; if reduced t nuch the patient 

is apt to suffer from insufficient elimination, which maj lead to 
uremia, and from nutritional failure due to I"-- of capillary pressure. 

Generally speaking, the first step is to secure resl and place the 
patient upon a milk and farinaceous diet. Attention to the intes- 
tinal tract is extremely important. Regular and free evacuation of 
the bowels is essential. This can generally be accomplished by a 
judicious regulation of diet, fluid intake, and exercise. When drugs 
are required liquid petrolatum, agar-agar, cascara, and other mild 
laxatives are often useful! The occasional employment of blue 
mass or calomel followed by a saline is often attended with exc< llent 
results. We cannot subscribe with enthusiasm to the laudatory 
results which are said to follow the use of the so-called intestinal 
antiseptics. The use of some of the various forms of fermented 
milk seems to be beneficial, chiefly, however, if other forms of 
dietary indulgence be limited. 

As has been pointed out there are two main groups of hyper- 
tensive cases: (1) Those presenting chiefly cardiac symptoms and 
usually dying a death from cardiac decompensation. In these 
cases the systolic pressure is very high; the diastolic pressure 
disproportionately less so. Exercise must be moderate and phys- 
ical overexertion avoided. Dietary restriction and eliminative 
treatment are not of vital importance. When drugs are required 
digitalis, strophanthin, ouabain, camphor with or without carbon 
dioxide baths give the best results. (2) Those with renal symptoms 
who die with uremic manifestations. In this group the diastolic 
pressure is disproportionately high (120-150). Pressure is to be 
reduced by mode of life, diet, purgation, sudation, venesection, etc. 

Some but by no means all the headaches of nephritis are due 
to high blood-pressure, and such cases as are, do not yield readily 
to therapy. Certainly direct treatment of the blood-pressure is 
neither justifiable nor successful, unless there is a distinct element 
of toxic vascular spasm which should be relieved by purgation or 
other eliminative means. The urgent symptoms of uremia are 
sometimes satisfactorily relieved by lumbar puncture and the with- 
drawal of cerebrospinal fluid or by venesection. 



314 TREATMENT OF ARTERIAL HYPERTENSION 

Focal Infections. Renal disease not infrequently results from, 
and i^ maintained by, focal infections. In all cases of hypertension 
careful search should be made for suppuration, especially in the 
gums, tonsils, and at the roots of the teeth. For the latter a com- 
petent x-ray examination is often necessary. The prostate gland, 
vermiform appendix and gall-bladder are also possible sites of 
infection. 

Purgation. Although drastic purgation has long been used for 
conditions associated with marked edema, ascites, and anasarca, 
the advisability of such therapeusis in cases of cardiac weakness 
lias been questioned. With a view to investigation of this problem, 
Neilson and Ilyland 1 carried out experiments with the blood- 
pressure, etc., after the use of different cathartics. 

After two doses of a purgative given in the morning, before 
food, the systolic pressure, which was chiefly affected, showed an 
average lowering of 17 per cent, (the diastolic 8 per cent., the 
pulse-pressure 24 per cent.), while the pulse rate increased 14 
per cent. Symptoms such as vertigo, chilliness, cold extremities, 
dyspnea, clammy skin, etc., were observed. Hypertensive cases 
showed the most marked results, and in these arrhythmia occa- 
sionally occurred. 

The results are presumably due to (1) loss of fluid from the 
blood; (2) unequal distribution of fluid, the splanchnic area, being 
chiefly affected, and a condition comparable to the experimental 
section of the splanchnic nerves having been induced; (3) cardiac 
weakness due to the small quantity of blood which the heart has 
to handle; increased viscosity; (4) the absorption of mineral salts 
from salines may have a direct action on the heart or its nervous 
mechanism. The fact that the pulse rate is sometimes decreased 
after such purgation despite the lowered blood-pressure tends to 
support this hypothesis. 2 

It was found that compound j<tl<)j> powder produced a more 
marked, constant, and prolonged fall of pressure than the salines, 
a reduction of 5 to 15 per cent, being generally demonstrable at 
the end of twenty-four hours. 

The milder laxatives are often useful in the reduction of arterial 
tension. They act by depleting the portal system and by removing 

1 The Effecl of Strong Purging on Blood-pressure and the Heart, Jour. Am. Med. 

L913, lx, 436. 

The intravenous injection of magnesium sulphate in cats leads to a sudden fall 

of pressure, and if the doaage is sufficiently large, to death. Hitter: Uebcr d. Einfluss 

v. Balzldsungen auf den Blutdruck, etc., Deutscb. Arch. f. klin. Med. Ohir., 1910, 

also McNider and Mathews, Airier. Jour. Physiol., 1907, xx, 323. 






SLEEP 315 

toxic materials which have irritant effects on the vascular walls 
and on the kidneys. The administration of ten grains of blue 
mass followed in six to eight hours by brisk saline purge is generally 
tin' most satisfactory method of treating the usual symptoms of 

hypertension such as headache, irritability, insomnia, palpitation, 
etc. Liquid petrolatum is often useful in producing alimentary 
evacuation. 

Enteroclysis is often beneficial for similar reason--, especially in 
cases of colonic stasis. 

Sleep. In many if not all cases blood-pressure falls during leep 
(often 30 to 50 mm.) and is associated with a diminished peripheral 
pulse wave. This fall of general arterial pressure is accompanied 
by a sustained and marked increase in the volume of the brain. 1 

Brooks and Carroll 2 found that tiigh.1 pressures were lower than 
day pressures in those who worked l>\ day, whereas the condition 
was reversed in night workers. Pressure variations of from 7 to 
4-1 mm. were observed. The least amount of fall occurred in those 
with already low pressures. The maximum full occurred aboul 
tin> hours after sleep began, the time at which insensibility is the 
greatest; and was followed h\ a gradual rise which attained it> 
maximum in the afternoon. Getting out of bed entailed only a 
slight temporary rise without materially influencing the regular 
cycle. Frequent interruption of sleep tends to prevent the full 
measure and suddenness of the primary fall of tension. If the 
primary drop occurs before the patient wakes it does not recur the 
same night no matter how sound the sleep. The amount of noc- 
turnal urinary secretion is apparently independent of the fall of 
pressure. Prolongation of the sleep interval does not produce 
lower tension. Nocturnal sleep, or even absolute rest, causes an 
average slowing of the pulse rate of twenty per minute as long as 
compensation is good. 3 

Some cases of insomnia show a reversal of the normal pressure 
relations, i. e., a higher pressure by night than by day. When 
sleep is produced by paraldehyde the pressure is reduced to 10 mm. 
below the normal individual sleep level. 4 

The nitrites are sometimes efficient somnifacients in cases of 
arterial hypertension, which is evidence in favor of the fact that 
the fall of pressure is a factor in the production rather than the 

1 Shepard, J. F.: The Circulation and Sleep, New York, 1914, p. 70. 

2 Proc. Assn. Am. Phys., 1912. 

3 Klewitz, F.: Der Puis im Schlaf, Deutsch. Arch. f. klin. Med., 1913, cxii, 38. 

4 Bruce: Edinburgh Medico-Chir. Soc, June 6, 1900, p. 156. 



316 TREATMENT OF ARTERIAL HYPERTENSION 

result lit' sleep. Most somnifacients owe their efficacy more to 
general nervous sedation than to depression of blood-pressure. 
The administration of bromides or chloral even in large doses does 
not increase the fall of pressure during sleep. Sleep may often be 
induced by warm baths, moist abdominal compresses, hot mustard 
foot baths, or gentle general massage administered two hours 
after the evening meal, which should be light in character. 

Insomnia is a frequent and troublesome symptom in hyperten- 
sive cases. Often it is the only symptom of which the patient 
complains. Successful results can only be obtained by a careful 
study of the individual case, but as a general rule the following 
factors should be eliminated or avoided: Concentrated mental 
work or strenuous physical exercise during the evening. Excite- 
ment of any kind whether by playing "Bridge," or otherwise. 
Excessive smoking or any coffee drinking after dinner. If strychnin 
or mix vomica is administered for therapeutic reasons the evening 
dos,s must be omitted. Business worries and household cares 
must be laid aside. 

Rest. Rest in bed for a week, with a milk diet is often the best 
remedy for reducing blood-pressure. It is likely that the mental 
relaxation thus brought about is more important than the physical 
repose. ( rumprecht called attention to the fall of pressure observed 
in laborers on entering the hospital, a result which he attributed to 
the unwonted rest. But it is also a fact that patients who take 
their worries and anxieties to bed with them show less improve- 
ment than do those who submit to the ordeal and succeed for the 
time being in throwing all responsibilities overboard, leaving their 
intellectual realm bordering on a temporary nirvana. This is also 
strikingly exemplified by the patient whose symptoms all disappear 
the minute lie leaves home for a vacation. 

Exercise. In ambulant cases of chronic arterial hypertension 
with good compensation the milder forms of exercise are of great 
benefit. Walking or golf are to be recommended, but with the 
warning that such exercise must be deliberate and that sudden, 
violent, or too prolonged efforts are harmful. The beneficial effects 
are attributable to a greater distribution of blood to the periphery, 

sudation, improved digestion and metabolism, as well as to the 

• list raction and psychic relaxation thus induced. Severe or sudden 
exercise such as heavy lifting, running or stooping must be avoided. 
Patients should be cautioned against straining at stool. The 
writer has seen disastrous retinal hemorrhages result from lack of 
this precaution. Severe physical exertion in man may raise the 



DIET 317 

blood-pressure from L10 to L80 nun., chiefly owing to the rise of 
intra-abdominal and intrathoracic pressure, 1 and it is more than 
likely that where hypertension exists, even greater increments of 
pressure maj occur. 

Diet. Overeating. The eating of F 1 which lias not hen 

earned by physical exercise, is one of the chief causes of arterial 

hypertension; hence the regulati >f diel plays an important 

part in treatment. The main indications are to restrict proteid 
food, especially meats; sail and substances capable of causing 
renal irritation (condiments, alcohol) or digestive disturbance. 
The diet should !><■ largely lactovegetarian, and limited in quantity 
so as to just supply the nutrient and caloric requirements. It is 
surprising on how small a ration metabolic equilibrium can be 
maintained in people pasl middle life. A high protein ration, 

it is true, even with an increased amounl of -protein nitrogen 

in the blood, does not appear to directly influence blood-pressure, 
but there are certain types of nephritis in which it is harmful and 
certainly it must throw additional work on the kidneys. 2 Tyrosin, 
an ammo-acid, formed in the digestion of meat, may be converted 
by the activity of the Bacillus aminophylus intestinalis into tyramin. 
The hitter substance possesses high grade vasoconstrictor properties. 
Prolonged fasting produces a gradual fall of blood-pressure which in 
Charteris's case amounted to 25 per cent, of the normal reading. 
The pressure returns rapidly to the normal after the resumption 
of food. 

In the case studied by Higgins in Benedict's 3 Laboratory, the 
general trend of both the systolic and the diastolic curves in both 
the sitting and in the prone posture was to decrease during the first 
fifteen days of the fast, systolic L34 to 94, diastolic 100 to 72 nun. 
Hg. This was followed by either a constant value or a slighl 
tendency to rise during the last part of the fast. 

The decline of the blood-pressure is apparently due to: (1) a 
decreased contractibility of the heart muscle, and (2) decreased 
vasomotor tone. The heart becomes smaller during the fast. Three 
days after the end of the fast, pressure was again normal. 

Thorough mastication and slow eating are essential. Neither 
mental nor physical exertion should be allowed immediately after 

1 McCurdy, J. H.: The Effect of Maximum Muscular Effect on Blood-pressure, 
Am. Jour. Physiol., 1901, v, 98. 

2 Frothingham and Smillie: "Different Nitrogenous Diets in Nephritic, " Arch. 
Int. Med., 1915, xv, No. 2. 

3 Study of Prolonged Fasting, Pub. Carnegie Inst, of Washington, 1915, 
p. 119. 



318 TREATMENT OF ARTERIAL HYPERTENSION 

food. Rest he/on 1 eating often materially assists the subsequent 
digestion. 1 

Blood-pressure rises after the ingestion of food, probably as the 
result of gastric distention; this is followed by hypotension, which 
corresponds to the time of active gastric secretion, and finally 
there occurs a second rise which is probably due to intestinal 
distention and plethora, and which is proportional to these factors. 
It is evident, therefore, that large, bulky, stimulating meals should 
be avoided in arterial hypertension. 

In an uncooked state certain foods may exert a direct effect 
upon blood-pressure, perhaps due to their effect on the thyroid 
gland. Liver substance fed to rabbits causes a 50 per cent, increase 
in pressure, and, according to Lubarsch, vascular lesions; while 
the administration of taurocholate or glycocholate of sodium 
causes a fall.' 2 

The question as to whether cardiac symptoms result from purely 
mechanical disturbances, such as alterations in blood-pressure, 
upward displacement of the diaphragm or the heart, or from reflex 
action on the part of the vagus, receives some elucidation from 
recent experiments. 

The abdomen is encircled by an inelastic bandage, and pressure 
(110 nun. Hg.) is exerted upon it by the inflation of a large rubber 
bag, observations on blood-pressure, together with radiographic 
studies of the diaphragm, being made. In health such a procedure 
produces a slight increase in the pulse and respiratory rate with a 
trifling fall of blood-pressure. In cardiopaths occasionally marked 
fluctuations of blood-pressure occur, but usually the results are 
closely akin to those produced in healthy people, showing that 
mere elevation of the diaphragm is of but little importance. Infla- 
tion of the stomach with air causes a slight fall, and with carbon 
dioxide, a rise of the diaphragm, chiefly on the left side. In health 
a slight rise of blood-pressure results from this procedure, in cardio- 
paths — especially in mitral disease— a marked fall of pressure (20 
mm.) occurs in about half of the cases, a fall which bears no relation 
to diaphragmatic displacement. 3 

It would seem, therefore, that gastric disturbances cause cardiac 



1 The question <>f diet Ikis been reviewed and ably discussed by Hecht: Ueber d. 
diatetische Beeinflussung pathologischer Blutdrucksteigerung, Ztschr. f. klin. Med., 
1912, lxxvi. 87. 

Van Leeraum, E. C: Alimentiire Blutdruckerhohung, Ztschr. f. exp. Path. u. 
Th.r., 1912, xi, 408. 

Kinidcr: l T eboi d. Kinfluss intraabdominaler Drucksteigerung u. des Fiillungszu- 
standes des Matins auf d. Blutdruck, Deutsch. med. Wchnschr., 1913, xxxix, 046. 



CONSERVATION OF ENERGY 319 

embarrassment chiefly through reflex and only secondarily through 
direct mechanical causes (see Tympanites, page 268). 

The main dietary rule is moderation. Meal in quantities up to 
100 or 150 gm. a day maj generally be allowed. The prejudice 
against red meat and eggs is unfounded. There is chemically bu1 
little difference between red and white meats. II' the amount be 
within the allowable limit it makes but little difference which the 
patient takes (see Nitrogen Retention, page 295). It is often neces- 
sary to restrict the use of sodium chloride, especially if the patient 
is edematous; for while there is no invariable absolute parallelism 
between salt retention and blood-pressure, the ingestion of salt in 
quantities greater than is demanded lor physiological equilibrium 
places unnecessary work on the kidneys. An absolutely salt-free 
diet is difficult to secure and excessively irksome to the patient, 
while the benefits derived from the same do not justify its adoption. 
Recent experiments indicate that the average individual consumes 
much more salt than is necessary for physiological equilibrium. 
This combined with the use of condiments leads to greater con- 
sumption of both food and fluid than is required for nutrition, and 
thus throws an unnecessary work on the eliminative organs. As a 
general rule both the number and the bulk of meals is to be reduced, 
and extractives, soups, gravies, etc., are to be avoided. The use of 
fruits and vegetables, especially if cooked, and if they do not cause 
flatulence or other symptoms of indigestion, is to be encouraged. 
Freshly made cheeses may be taken, but those whicb have l>ccn 
ripened must be avoided, since they contain oxyphenylethylamin, a 
bacterial decomposition product with marked pressor potency and 
identical with one of the toxic bases to which ergot owes its effects. 1 

Conservation of Energy. — In the early stages of increased blood- 
pressure the proper regulation of the daily life and diet is the only 
rational or efficacious method of treatment. The avoidance of 
hurry and worry are of prime importance, and these factors are 
often the most difficult matters to correct. The patient should 
understand that the "doing of things against time," the attention 
to several things at once, the ceaseless mental concentration upon 
different problems, the assuming of unnecessary tasks and responsi- 
bilities, the frequent interruption of a train of thought by telephone 
calls, etc., are unwarranted drains upon vital energy, and that he 
who leads the high-pressure life is a physiological spendthrift who 
is bound to end in early bankruptcy. This applies with special 
emphasis to that class of high-strung individuals who "go on their 

1 For literature see Edit. Jour. Am, Med. Assn., October 17, 1914. 



320 TREATMENT OF ARTERIAL HYPERTENSION 

nerves," and who. as Holmes lias said, "put energy out at interesl 
and receive nervous derangement in return." "Worry, suspense, 
anxious anticipation, disappointment, consciousness of failure or 
of failing health, the hunted feeling that comes of overwork, and 
arrears, regret, sorrow, despair"- ''wear out not only the nervous, 
but also the cardiovascular system." (Bruce.) 

Fluid. Too much fluid throws an unnecessary burden on the 
kidneys. The old idea of flushing out the system, of diluting toxic 
products, etc., in patients already dropsical has been shown to be 
erroneous. The total intake, in whatever form, should in non- 
dropsical patients not exceed or fall below two liters per diem. 
A tumblerful of hot water flavored with lemon juice or rind, or 
with the addition of citrate of potassium, between meals ami at 
bedtime is often beneficial. It is sometimes, although rarely, 
advisable to diminish the fluid intake even in cases free from 
dropsy. This should not be done if there is nitrogen retention in 
the blood. A morning draught consisting of potassium nitrate, 
grs. xx, sodium nitrate, grs. \-2, and potassium bicarbonate, grs. xx, 
in a tumblerful of water, has been recommended by Sir Lauder 
Brunton. 

Ilogan 1 has administered intravenously, saline solution containing 
sodium carbonate (20 gm. cryst., 2000 c.c.) in cases of high blood- 
pressure associated with uremia and believes that he produced a 
marked fall of pressure, with sudation and symptomatic ameliora- 
tion. He explains this as due to the fact that if the concentration of 
the infusion is right, "the tissues and blood colloids are robbed 
of their water, and while tissue edema and high blood-pressure are 
decreased, free water is made available for excretion as urine, sweat 
and intestinal fluid." 

Alcohol is contra-indicated. In small well-diluted doses it may 
do no great harm, but when possible it should be eliminated entirely. 
The use of tobacco should be restricted. Smoking causes more 
mailed increase of blood-pressure in hypertensive than in normal 
subjects. This rise of pressure is not infrequently associated with 
palpitation, vertigo, insomnia, nervousness, precordial distress, 
and tremor' (see Tobacco and Blood-pressure, page 235). 

Hydrotherapy. Warm hut lis- are valuable depressor remedies, 
and an occasional Turkish or electric-light bath is often useful, 
although these procedures must never be prescribed without due 

1 Alleged Danger of Intravenous [njections in High Blood-pressure, Lancet-Clinic, 
January _'. L915. 

•Barazzoni, C: Cura dell' ipertensione arteriosa mediante la D'Arsonval- 
izzazione, Gaz. med. [taliana, L0O5, lvi, 113. 



HOT BATHS 321 

consideration of the possible deleterious effects, i. e., marked 
temporary increase in blood-pressure before sweating occurSj 
vascular rupture, cardiac strain, and reduction of nervous tone. 
Saline baths (one pound of washing soda or sodium chloride to the 
tnh) are more stimulating and produce more marked sudation. 
Nauheim baths are especially useful if there be cardiac dilatation 
or weakness. 

A g I sweat often causes a ID to I'll nun. fall in pressure, which 

tends to last throughout the day, especially it' the procedure be 
repeated daily. Occasionally, for reasons nut yet understood, a series 
of sweats will reduce the pressure for weeks or months. This 
method of treatment is of course specially indicated if there he renal 
insufficiency or threatened uremia, bul the occasional employmenl 
of sweat-producing hydrotherapy is often advisable in the absence 
of these conditions. Just how it does good in uremia is uncertain. 
The amount of urea eliminated through the skin even with a copious 

sweat cannot exceed 111 to 15 grains, and it is improbable that other 
toxic products are thrown oil' in any greater proportions, h has 
been shown that the relative concentrating power of the skin and 
kidney for urea and ammonia are very different, though in each 
instance the values are higher than in the blood. 1 Further investi- 
gations may teach its that, depending upon the character of the 
toxin to be eliminated, sweat baths may he definitely indicated 
or contra-indicated in a given case. The beneficial effects are 
probably brought about by a change in the mass movement and a 
redistribution of the blood, especially that in the splanchnic domain; 
the peripheral arterioles and capillaries being temporarily dilated 
and flushed with blood. According to Amblard, electric-light baths 
produce less primary rise in pressure, and are therefore to be pre- 
ferred. 

After the sweat the patient should be allowed to cool off gradu- 
ally, being first wrapped in blankets, and after a time sponged 
or sprayed with cool water or alcohol. A sudden plunge in a cold 
pool or immersion under a cold shower bath, especially while the 
patient is still actively perspiring, may produce an increase of 50 
mm. in blood-pressure, an occurrence which throws a tremendous 
strain on the cardiovascular system. 

Hot Baths. — " (1) Baths with a temperature below the indifferent 
zone (33° to 35° C; 91.4° to 95° F.), produce an increased blood- 

1 Plaggemeyer, H. W., and Marshall, E. K. : A Comparison of the Excretory Power 
of the Skin with that of the Kidney through a Study of Human Sweat, Arch. Int. 
Med., 1914, xiii, 159. 
21 



322 



TREAT MEXT OF ARTERIAL HYPERTEXSIOX 



pressure, lasting throughout the bath, with a decrease in the pulse 
rate. (2) If the temperature be approximately 40° C. (104° F.), 
after a short initial rise, a lowering of the blood-pressure to or below 
the normal occurs; this lowering is then followed by a second 
increase in the pressure. Below 37° C. (98.6° F.), the pulse rate 
is lowered, above this point it is increased. (3) Baths over 40° C. 



TIME IN MINUTES 
20 30 40 50 60 



120 





110 


(3 




100 


5= 


111 




5 


5w 


80 


z 








< 




hi 




</> 


K 


maa 


-80 


3 


5 


O- 


■J> 


■-37° 


70 


■x 



A 


^77$f\ 


/ \J_ ^^ J^*~ 


.'-''ji ^S" 


^ \~Z^ 


* 







■■■SYSTOLIC 

VBLOOD PRESSURE 
DIASTOLIC) 

PULSE PRESSURE (AMPLITUDE) 

._ PULSE RATE 

BODILY TEMPERATURE C. 



Fi<;. 101.— Chart showing the effect of a tub bath of 41° C. (105° F.) upon the 
blood-pressure, pulse rate, and bodily temperature. The vertical lines indicate the 
beginning and cud of the bath. (After Strassburger.) 

(104° F.), produce an increase in pressure lasting throughout the 
entire bath, with an increase of the pulse rate." 1 

Hot baths may produce weakness, syncope or anginoid pains in 
arteriosclerotic subjects, if the temperature be too high or the 
immersion too long. Kerr, 2 who has reported some eases, attributes 



1 Muller, <>., and Forcbbeimer: Therapeusis of Internal Diseases, iii, G18. 
" 'Ili«- Danger of Bathe in Patients Suffering from Arteriosclerosis, California State 
Jour. Med., July, 1916. 



I OLD B ITHS 323 

the anginoid attacks to the increased pulse rate and the increased 
cardiac load which results from a marked lowering of the diastolic 
pressure. Hot-air, steam, and electric-lighl baths exercise effects 
proportional to their temperature. Hot baths musl be employed 
with caution in the treatment of hypertension in diabetes. It has 
been shown that if the bodily temperature he raised either by fever 
or by artificial means the sugar content .if the blood increases. 1 

Foot Baths. — Hot foot baths, to which mustard may he advan- 
tageously added, are often a satisfactory treatment for the headache 
and insomnia of hypertension. If the patient is to sleep, the feel 
must be kept warm, and for this purpose a hot-water bag in bed 
is often desirable. 

Cold Baths.- The application of cold, especially in the form of 
forcible sprays and douches (mechanical stimuli), increases blood- 
pressure. The lower the temperature and the more sudden the 
application, the greater the rise. A sudden plunge into a cold pool, 
accompanied by the additional muscular efforts of swimming, 
produces a great increase in pressure, quite sufficienl in arterio- 
sclerotic cases to cause vertigo and precordial oppression, to pre- 
cipitate an apoplexy, an attack of angina pectoris, or of pulmonary 
edema. 

In normal individuals the vascular reaction /<> //<"/ mul cold&re 
general reactions, i. e., a cold hath reduces peripheral blood How 
and temperature, not only in the parts immersed hut elsewhere. 
Even sitz baths have a similar effect, although the idea still persists 
in some minds that blood is simply crowded out of the area to 
which the cold is applied and forced into other peripheral areas. 
This has been shown to be incorrect. In abnormal conditions, 
how T ever, whether functional or organic in origin, local peripheral 
variations may occur. The peripheral application of cold produces 
cerebral hyperemia, whereas heat has the opposite effect. It 
also decreases systolic output, whereas hot baths increase the 
latter. It should be remembered, however, that where sensory 
stimuli (friction, C0 2 , etc.) are added to the cold bath the systolic 
output may be increased despite the low temperature of the bath. 
Following a cold bath the reaction becomes reversed, the systolic 
output is increased and peripheral vascular dilatation occurs. 
When the circulatory apparatus is efficient or if the cold bath has 
been preceded by sweating, etc., the reversed reaction may set in 
even while the subject is still in the cold bath. The changes in 

1 Roily, F., and Oppermann: Das Verhalten des Blutzuckers b. Gesunden u. 
Kranken, Biochem. Ztschr., 1913, xlvii, 187. 



324 TREATMENT OF ARTERIAL HYPERTENSION 

blood-pressure which result From sensory or thermic stimuli are 
dependent both upon the state of the splanchnic veins and upon 
that of the peripheral arterioles. Blood-pressure may increase 

despite splanchnic dilatation as a result of peripheral contraction 
(cold baths, etc. i, so long as the splanchnic vessels retain their 
tone. 

A cold hath is by far the most potent remedy which we possess 
for altering blood distribution. It adds, however, a distinct burden 
upon the heart. Spray and shower baths still further increase 
the burden by the sensory stimulation which they provoke. If 
the heart is weak, instead of a rise in pressure, cold baths may 
actually cause a fall, because the heart weakens instead of responding 
to the call for increased effort. Indeed, syncope and sudden death 
may thus he precipitated. Nature, it appears, often wards off the 
latter events by rendering vasomotor nerves reactionless. 

0. Miiller has shown that not infrequently the peripheral 
arteries of cardiopaths are plethysmographically irresponsive to 
the local application of ice. It must be remembered, however, 
that although this may be true for minor reactions, such as those 
just mentioned, nevertheless a major reaction such as that produced 
by a cold bath may be suddenly fatal. With diseased arteries 
the sudden elevation of pressure which follows a cold bath may 
produce vascular rupture. 1 

Too frequent or too vigorous hydrotherapeutic measures tend to 
lower nerve fane and may do actual harm. In the thin, high-strung, 
hypertensive patient they must be used with caution. Too violent 
forcing down of the arterial pressure by means of baths, etc., is 
jusl as reprehensible as when the same end is attained by means of 
the nitrites. If the patient feels listless, weak, or exhausted, as a 
result of the baths, they are doing him harm, despite the fact that 
his pressure may be more nearly normal. Cold baths although 
increasing the arterial, lower the capillary, blood-pressure. The 
effect of hot baths upon the capillary pressure is less constant 
(Landerer). 

Carbonated Brine Baths. Despite the fact that Miiller and Weiland 
have furnished plethysmographic evidences of peripheral vaso- 
constriction, and Liwschutz tachographic indications of an increased 
systolic output, it must be confessed that in a large number of 
cases treated with carbonated brine baths no constant pressure 

effects can be demonstrated. 

1 This Bubjecl has hern admirably summarized by <). Miiller and E. Veiel: Samml. 
klin. Vortrage, 1909 10, X. !•'., l ♦ .7" L96 (innere medizin), i>. (ill. 



C IRBOA i FED BR1 VE BATHS 325 

The pressure at the end of the bath or upon the completion of 
the treatment, in cases cither of hypertension or of hypotension, is 
variable. On the whole, pressure is more frequently raised than 
lowered, but it is impossible to know beforehand in which way a 
given case may respond. 1 J. II. Pratt 2 found that in patients with 
normal or only slightly insufficient heart-, carbon dioxide baths 
(95° to 85° F.), usually raised systolic pressure. The pulse rate. 
while usually lowered may be increased. There is no relation 
between the effect of baths upon these two factors. In normal 
subjects identical successive baths may have diametrically opposite 
results in the same individual. The pulse-pressure is often bul not 
invariably increased by cool carbon dioxide baths; it may, however, 
be decreased. We do not mean to derogate the usefulness of this 
form of treatment, which is often followed h\ excellent re ults, 
especially in cases of cardiac weakness, but merely to point out 
that neither the subjective nor objective improvement rests on a 
basis of blood-pressure change. 

Even less marked and less constant results are observed after 
the use of alternating current baths. 3 

The organism reacts to electric stimulation faradic, galvanic 
or alternating currents) by a negative volume change as shown by 
the plethysmograph. The effect upon the pulse rate and the blood- 
pressure is inconstant both in the same and in different individuals. 
Whether the benefits which sometimes follow electric baths in 
cardiac disease are due to cutaneous reflexes or to muscular ion- 
traction is uncertain. 1 

The effects of the baths depend largely on the temperature. If 
below 33° to 35° C. (92° to 05° F.) the pressure will be more apt to 
rise, if above this point, to fall. But with temperatures above 
40° C. (104° F.) the pressure first rises and later falls. Hot and 
cold douches elevate and lukewarm douches lower tension, d he 
effect on the pulse rate is equally important, heat accelerating and 
cold retarding it. These effects are generally transient, not lasting 
more than an hour or two. 

Exception is often taken to the fact that carbon dioxide baths 
are used both in the treatment of arterial hypotension and hyper- 

1 Swan, J. M.: The Influence of Carbonated Brine (Nauheim) Baths on Blood- 
pressure, Arch. Int. Med., 1912, x, 73. 

2 Action of Carbon Dioxide Baths on the Blood-pressure in Cardiac Disease, Tr. 
Am. Climat. Soc, 1913, xxix, 252. 

3 Laquer, A. : Ueber d. Verhalten des Blutdruckes nach Kohlensaure u. Wechsel- 
strombadern, Ztschr. f. exp. Path. u. Therap., 1909, vi, 855. 

4 Geissler: Der Einfluss Elektrischer Reize auf d. Blutvertheilung im Mensch- 
lichen Korper, Munchen. med. Wchnschr., 1908, lv, 92. 



326 TREATMENT OF ARTERIAL HYPERTENSION 

tension. Their beneficial effects, which are unquestionable, are 

to be explained thus: The baths have essentially a cardiovascular 
tunic effect. Ordinarily they are followed by a rise in blood-pressure, 
an increased systolic output, and a slowing of the pulse. This 
leads to a generally improved circulation, nutrition, and excretion, 
ami may indirectly lower bloods-pressure, especially in cases of 
high-pressure stasis. Their action is thus comparable to that of 
digitalis. Those most competent of judging, state that these baths 
are harmful in cases of advanced renal lesions. This is probably 
due to the temperature (83° to 90° F.) to which the baths are 
lowered, for certainly the secretion of sweat and urine is distinctly 
increased in the average case to which this treatment is given. 

( k>ol carbon dioxide baths slow the heart and cause contraction 
of the peripheral arterioles. The thick layer of bubbles which 
surrounds the body in part prevents the loss of heat which occurs 
in ordinary cool baths, thus causing a pleasant sensation of warmth. 
Warm carbon dioxide baths increase the pnlse volume, but have 
the opposite effect from cool baths upon the arterioles. Since 
these baths make considerable demands upon the circulation they 
must only be given under medical supervision. 

Oxygen Baths. — Oxygen baths have been extensively employed 
as a remedial measure in cases of arterial hypertension, and are 
said by numerous observers to be attended with very satisfactory 
results. A lowering of tension is more constant than in the case 
of carbon dioxide baths. These baths are contra-indicated in the 
terminal hypotension of arteriosclerosis (Winternitz), 1 especially if 
associated with anemia (Baedeker). 2 

The baths which may be administered at home 3 are given at a 
temperature of !>()° to 95° F., for from ten to twenty-five minutes. 
A course of baths (twenty-four) should be given on successive days, 
with occasional intermissions, either in the morning or at night 
(for insomnia), but not too soon after a meal. 

Precordial Aplications. — The application of cold to the precordium 
both experimentally and clinically 1 tends to slow the heart rate, 
to increase blood-pressure and to diminish systolic output. These 
changes arc produced in part reflexly and in part directly through 
reduction of the myocardial temperature. The increased pressure 

1 Blatter f. klin. Hydrother., 1907, p. 1. 
Ther. '1. Gegenwart, 1910, p. 2. 

» "Perogen" baths. Morgenstern .t Co., New York. The oxygen is liberated by 
t lie admixture in the hath of two powders (sodium perborate ami magnesium borate). 

' Eirschfeld, V. and Lewin, II.: (Jntersuchung ueber die Wirkung <les Herzsch- 
lanches, Ztschr, f. Physik. u. Diat. Tberap., L914, xviii, 6. 



BANDAGING OF THE EXTREMITIES 327 

is secondary to vascular contraction. Hot precordial applications, 
on the other hand, raise blood-pressure despite peripleural vaso- 
dilatation and this is probably due to an increased systolic output. 
It is obvious therefore that the application of ice-bags may be 

injurious to a diseased myocardium which is already pushed to its 

limit while in the same case the local use of heat might be directly 
beneficial. 

Phlebotomy. -Venesection is one of the most prompt and effica- 
cious methods of lowering blood-pressure and reliev ing a distended 
right heart. Its beneficial effects in uremia are generally attributed 
to the foregoing effects and not to the amount of toxic material 
which is removed from the blood stream. Phlebotomy is chiefly 
indicated in conditions of venous stasis, whether due to right or 
left ventricular weakness. It often yields excellent results in the 
treatment of aortic aneurysm and of acute pulmonary edema. In 
order to obtain definite results 300 to 500 c.c. of blood must be 
withdrawn. 1 A rapid venesection amounting to from '.)()() to ")()() c.c. 
will generally reduce blood-pressure Prom 5 to 30 mm. Asa rule the 
more rapid the withdrawal the more pronounced the fall of press- 
ure. The symptomatic relief afforded is sometimes immediate — 
even before an appreciable quantity of blood has been withdrawn. 
This fact shows that mere section of the vein produces some 
definite reflex action probably through the medium of the nervi 
vasorum. 

Bandaging of the Extremities. — The application of tourniquets to 
the extremities with sufficient constriction to prevent venous 
outflow, although allowing arterial inflow, has temporarily much 
the same effect upon the system as a phlebotomy. It has been 
recommended as a method of treating heart weakness, but has 
not found much favor. If too much pressure is exerted, inhibition of 
arterial inflow and marked increase of general blood-pressure will 
result. The method must, of course, not be applied in the presence 
of edema or varicose veins of the extremities. Relaxation of the 
bandages must always be gradual so as not to suddenly increase 
cardiac work. By bandaging all four extremities 20 per cent, of 
blood can be removed from the general circulation and the heart 
spared a corresponding amount of energy. Subjective symptoms 
are said to show a distinct amelioration. 2 This procedure has 
been useful in cases of threatened pulmonary edema and other 
conditions associated with increased venous pressure. Pronounced 

1 Moritz and Tabora: Verhandl. d. Kong. f. inn. Med., 1909, xxxvi, 378. 

2 Lillienstein : Der unblutige Aderlass, Phlebostase, Med. KLinik, 1912, vii, 316. 



328 TREATMENT OF ARTERIAL HYPERTENSION 

passive congestion in the extremities may cause a fall of 20 mm. 
Hg., sometimes rather suddenly, with signs of collapse. 

High-frequency Currents. 1 — Although there is as yet no unanimity 
of opinion on the subject, some very favorable reports have been 
published regarding the efficacy of high-frequency currents for the 
reduction of high arterial pressure. The current is said to act 
by lowering peripheral resistance and also by acting as a cardiac 

tonic. 

Nagelschmidt, 2 who reports good results in a series of 120 cases, 
believes that the discrepancies in the results attained by different 
observers with the high-frequency current are due to the fact that 
an insufficient amperage has generally been employed. 

The exact means by which high-frequency currents reduce blood- 
pressure are not thoroughly understood. The belief at present 
is that the effect is mainly thermal (local heating, rise of bodily 
Temperature, and pulse rate, sudation and peripheral vasodila- 
tation! and that it is not due to cardiac depression. 

'• If two electrodes from a galvanic or a faradic current are placed 
in a bowl of water, decomposition occurs with bubbles at either 
pole. Even if quite weak, a hand placed between them experiences 
painful electrolytic sensations. If these electrodes are replaced 
by high-frequency ones, hardly any electrolysis occurs. The water 
merely gets warm, and a hand placed between them experiences no 
sensation whatever excepting that of warmth, even with currents 
so strong that were they galvanic or faradic they would cause 
chemical and electrolytic changes capable of destroying the tissues" 

iT). 3 

''With regard to alterations in the blood itself, we may look 
upon the action of high frequency in reducing blood-pressure as 
being in some way analogous to the action of a rise of temperature, 
when, unless there is dyspnea and cyanosis, the rapid metabolism 
caused by the onset of any fever is always accompanied by a fall 
in blood-pressure, an increased excretion of uric acid, and a quick 
capillary reflux, exactly what happens on a small scale with a dose 
of high frequency." 

Ubo -,-i en oi as Arsonvalization after d'Arsonval, to whose physiological studies 

ttUC h of our present knowledge od the subject is due. For further ...formation 

regarding ^- history, electric data, detailed description and iterature on this sub- 

j( .„ ^ Ulen, W. C: Radiotherapy and Phototherapy, Phdadelplua 1904 -Mann, 

L • Krause and Gane's Lehrbuch d. Ther. Inneren Krankheiten, 1911, >,488, 509. 

, Diathermic Treatment of Circulatory Disorders, Arch. Rontger. Ray, February, 

' The Effect ol Electrical Currents upon Blood-pressure, British Med. Jour., 
October 8, L910, p. L052. 



HIGH FREQX I \< ) CI RRENTS 329 

The effect on the nervous system is definite, bu1 the sensory and 
motor stimuli are too rapid to permit of a response, " for all elecl ric 
vibrations beyond ten thousand per second lie beyond the limits 
of the range of frequencies to which these nerves can respond. 
Although no dired effects can be demonstrated, yel their applica- 
tion to any muscle or nerve does in some wa,\ affeel it, for it is 
found afterward that its excitability to all ordinary electric gal- 
vanic and faradic) stimulation is lessened" (Sayer). The high- 
frequency currents act specially upon the nerves of the vasomotor 
system, the splanchnics and the large sympathetic trunks and 
the greatest effects arc produced if the current is passed through 
these tissues. In nerves containing both constrictor and dilator 

fibers, ordinary electric stimulation produces a i •<■ marked effect, 

especially if weak current- are employed (('rile). 

Method of Application. I. Induction. The patient is placed 
in the centre of a wire cage, through the wires of which the current 
is passed. An induction current is thus generated in the patient. 

The presence of such a current can be demonstrated by means 
of an incandescent globe, held in tin- hand of the patient, which 
without any direct connection with the solenoid will become 
luminous (Mann). 

II. Condensation. — When the patient rests on an insulated couch 
or chair cushion, a high-frequency current derived from a static 
machine, or preferably from a specially designed apparatus, is 
passed through his body, using either a monopolar or a bipolar 
method (the patient being- connected with the circuit by one or 
two pole electrodes, and acting as a current condenser). The 
strength of the current passing through the coil is gauged by an 
amperemeter, while the amount received by the patient can be 
gauged with a milliamperemeter placed between the table and the 
couch. Burch 1 has reported untoward results in some cases. He 
found that if patients who scarcely responded to from 20 to 50 
milliamperes were subjected to 200 to c.00 milliamperes a very 
marked fall of pressure with signs of collapse sometimes occurred. 
Patients who readily respond to the smaller dose are, he believes, 
instances of spastic hypertension which cannot safely be treated 
w r ith the heavier dosage. The cases that show no response to the 
milder current show T the best results under the larger dosage. These 
cases are supposedly due to both a vasomotor spasm and a vascular 
degeneration with a relatively strong heart. 

■ 1 Electrical Treatment of Arterial Hypertension, Med. Record, 1911, lxxx, 866. 



330 TREATMENT OF ARTERIAL HYPERTENSION 

III. Local Application. (Diathermic Method.) — By means of 
electrodes of different kinds the current is conducted from a small 
solenoid to the patient. In order to insure greater penetration and 
to minimize the local effect which this mode of application chiefly 
favors, the current is taken from an alternating current generator 
and then interrupted by means of a jump-spark attachment. The 
action of this (diathermic) current is somewhat different from 
that of d'Arsonval (Mann). There is no cutaneous resistance. 
The current passes from one electrode to another by the shortest 
route, permeating the intervening tissues with practically equal 
intensity. It is claimed that blood-pressure can be (1) raised, by 
precordiodorsal application, as the result of cardiac stimulation 
and cutaneous irritation, and (2) lowered, through peripheral 
dilatation, by application to the central nervous system (medulla). 
When one desires to heat the heart muscle itself, the large indifferent 
electrode is placed over the dorsal region, the smaller, movable 
one over the precordium. The latter must be so constructed that 
it is possible to pass 1000 to 1200 milliamperes for at least five 
minutes without undue heating of the skin (Nagelschmidt). 

Indications. — High-frequency currents yield the best effects in 
cases of spastic hypertension with relatively good heart muscle 
and kidneys. The effects produced are said to be more lasting 
than those resulting from the use of vasodilator drugs. They can 
lead to permanent benefit only when coupled with hygienic and 
dietetic correction. Too great a fall of pressure as the result of 
such therapeusis may, according to Moutier and Challamal, 1 be 
counteracted by the application of this current to the vertebral 
column. According to Fontana 2 the variable results obtained by 
high-frequency currents upon blood-pressure depend upon the 
permeability of the kidneys. The vascular dilatation and increased 
metabolism which the current produces throws extra work on the 
kidneys which, if these organs are functionally active, causes a 
fall of blood-pressure, whereas insufficient kidneys fail to react 
and blood-pressure remains high. 

Massage. Although the primary effect of massage, as the result 
of cutaneous stimulation, tends to raise blood-pressure, this effect 
is more than counter-balanced by its effect on lymphatic and venous 
flow. Good general massage, especially in association with Swedish 

1 De l'abaisscnicnt de la pression arterielle au dessous de la normale par la d'arson- 
valization, Coxnpt. rend. Acad. d. bcL, Paris, 1905, cxl, 742. 

* Dell'azione delle correnti ad alia frequenza Bulla pussione arteriosa in rapporto 
alia permeabilita renale, Gazz. d. Ospedali e. d. Clin., 1914, xxxv, ">_'.;. 



CUTANEOUS IRRITATION 331 

movements, is one of the most useful measures which can be employ ed 
in the treatment of arterial hypertension. It supplies manj of 
the benefits of exercise without tbeattendanl expenditure of energj . 

Abdominal Massage. Some authorities hold thai this form of 
massage is contra-indicated in cases of hypertension and cardiac 
disease. Experimentally in animals it increases blood-pressure, 
but some clinical observations show that this is by DO means always 
the ease. Indeed, a fall of pressure may be observed. Certainly 
compression of the large abdominal arteries tends to raise the 
genera] pressure al least temporarily, bu1 generally (with judicious 
massage) this rise is slight and is soon more than counter-balanced 
by the good effect which the manipulations have upon digestion 
and intestinal peristalsis. 

When skilfully performed it has a generally sedative effed accom- 
panied by a slowing of the pulse and often a fall of blood-pressure, 
probably by its influence on local stasis in the mesenteric vessels, 
although vagus action may have a part in the results. 1 

Vibratory Massage. This form of massage yields good results, 
requires less time, and does not uecessitate undressing, but, as a 
therapeutic measure, it is less satisfactory than good general 
massage with passive movements. A valuable factor of the latter 
procedure lies in the hour's rest and relaxation which the patient 
should be instructed to take after its completion. Even prolonged 
vibration of the precordium is without effect upon the pulse rate, 
the blood-pressure, or the systolic output. 2 It has been claimed 
that definite blood-pressure-lowering effects can he obtained by 
concussion of the seventh cervical vertebra for a period of about 
five minutes, and that vibration of the sixth and seventh dorsal ver- 
tebras tends, although less constantly, to increase vascular tension. 3 

Cutaneous Irritation. — Local irritation of the skin (mustard, 
capsicum, etc.), produces redness by dilatation of the capillaries 
and venules without a corresponding dilatation of the underlying 
arterioles. 4 Such methods of counter-irritation find a distinct field 
of usefulness when applied to the feet, neck, or precordium in helping 
to relieve some symptoms of hypertension (insomnia, headache, 
precordial and epigastric oppression) as well as in mitigating the 
restlessness and delirium of acute infections, notably of pneumonia. 

1 Ekgren, E. : Ueber den Einfiuss d. Abdom. Massage auf Blutdruck, Herzthiitig- 
keit u. Puis, etc., Ztschr. f. diatet. u. physik. Therap., 1902, v, 191. 

2 Plate and Bornstein: Ueber d. Einfluss d. Herzvibration mit hoher Frequenz 
auf d. Kreislauf, ibid., 1913, xvii, 65. 

3 Abrams, A.: Spondylotherapy, 1910, p. 248. 

4 Wood and Weisman: Arch. Int. Med., September, 1912. 



332 TREATMENT OF ARTERIAL HYPERTENSION 

Passive Exercises. — This form of gymnastics administered either 
by an attendant or by machinery (Zander apparatus, etc.), since 
it supplies the beneficial effects of muscular exertion without an 
attendant expenditure of volitional nervous energy, tends to lower 
blood-pressure in a satisfactory manner, and is a useful adjunct 
t<> other forms of treatment. 

Climate. A warm, equable climate is desirable. Winters may 
he -pent in Egypt, Jamaica. Bermuda, Southern California, etc. 
Moderate warmth and sunshine conduce to outdoor exercise which, 
when accompanied by gentle perspiration, is most desirable, but 
sudden chilling must be sedulously guarded against (see Altitude). 

Psychic Treatment. Certain types of high-pressure individuals 
are extremely susceptible to suggestion, and tend to become intro- 
spective. Cautionary advice in such instances must be tempered 
with encouragement. The additional element of self-worry must 
not be added to their other burdens. For this reason it is often 
inadvisable to tell the patient anything about pressure changes, 
particularly if these should happen to be for the worse. The 
beneficial effects of light exercise and diversions of different kinds 
owe much of their good effect to psychic impressions. 

Respiratory Gymnastics. — In certain cases of hypertension both 
symptomatic improvement and lowering of tension may be induced 
by breathing exercises. Space will not allow discussion in detail of 
the mechanism by which this is brought about; but such results 
are not difficult to understand when we consider that better aeration 
of the blood diminishes its centrally pressure-raising CO2 content. 
Proper action of the respiratory muscles, especially of the diaphragm, 
facilitates blood flow to and from the heart, and increases venous 
and lymphatic How in the digestive organs and elsewhere. Thus 
tissue metabolism and elimination are directly favored. 

That the question is not, however, a perfectly simple one is 
shown by Stewart's investigations, which proved that peripheral 
blood flow fin the hands) was diminished by dee]) breathing. 

"The cause of the diniiiiut ion in blood flow produced by forced 
respiration is without question in part a mechanical effect on the 
action of the heart due to the changes in the intrathoracic pressure. 
Hill and Flack have stated that the left ventricle becomes smaller, 
as shown by Koutgen-ray pictures, the radial artery emptier, 
and the arterial blood-pressure lower with each forced thoracic 
inspiration. That a chemical change may also be concerned is 
indicated by experiments in the case of cyanosis already mentioned, 
in which oxygen inhalation distinctly increased the blood flow 



RADIO ACTIVE SUBSTANCES 333 

in the hand without affecting the respirator} movements <»r tin- 
total pulmonary ventilation, while in norma] persons it bad no 
such effect. It in;i> I).- thai the washing ou1 of the carbon dioxide 
by the forced respiration causes, even in such shorl experiments 
and with such moderate exaggeration of the respiratory movements, 
those changes in the distribution of the blood, particularly its 
accumulation in the great veins, which Henderson associates with 
'acapnia,' and which, according to him, are so important a factor 
in surgical shock. Other vascular changes for example, a diminu- 
tion of the How in the coronary circulation due to the fall of pressure 
in the aorta, which aid the mechanical changes in the thorax in 
decreasing the average output of the heart may occur. Changes 
produced through the vasomotor centre on the peripheral vessels 
may also play a more direct part. This is at any rate suggi ted 
by the fact that the perceptible change in the How caused by forced 
breathing is not the same for the two hands, as it mighl he expected 
to be were the whole effect a cardiac one. However, it is not 
intended to lay much stress on this suggestion, for the initial 
differences in the How in the two hands arc not sufficiently great 
to permit without hesitation the application of this criterion. The 
beneficial influence of oxygen on the How in the case of cyanosis 
may be explained as the result of the oxygen action in diminishing 
the excitability to carbon dioxide of the vasomotor cent re and other 
mechanisms affected by hypercapnia." 1 

Differential pressure in the lungs, breathing into rarefied air, 
has been used as a method of promoting blood-circulation. Bruns 
found that when the pressure of the air into which the patient 
breathes has been reduced to 8 to 10 c.c. IU), both pulse and 
respiratory rate increase, peripheral flow, as shown by the plethys- 
mography is increased and venous pressure falls. - 

Radio-active Substances. — Our knowledge of the physiological 
effects of radio-active substances is very meager. The employ- 
ment of these remedies is still in its experimental stage, and there 
is considerable evidence to show that the efficient therapeutic dose 
and the toxic dose are separated by but a narrow margin. 

The drinking of water charged with radium emanations appears 
to increase tissue metabolism, the activity of ferments and urinary 
flow. Good results attending its administration in cases of gout and 

1 Stewart, G. N. : Studies on the Circulation in Man, III. The Influence of 
Forced Breathing on the Blood Flow in the Hands, Am. Jour. Physiol., 1911, xxviii, 
No. 3, p. 196. 

2 Bruns, O.: Die kunstliche Luftdruckerniedrigung u. d. Lungen, etc., Miinchen. 
med. Wchnschr., 1910, hoi, 2169. 



334 TREATMENT OF ARTERIAL HYPERTENSION 

of arterial hypertension have been reported. It is now generally 
believed that the beneficial effects obtained at certain health 
resorts such as Bad Gastein in the Austrian Tyrol, and Hot Springs, 
Arkansas, are due to the radio-active waters there present. 

Water charged with radium emanations, however, quickly loses 
its potency and hence bottled waters are inert. The artificial 
charging of water with radium emanations is now, however, possible, 
and favorable results may be obtained with home-charged water 
having a potency of 5000 to 20,000 Mache units when taken over 
prolonged periods of time. 

Solutions of thorivm-X have been administered intravenously. 
Plescb, who employed this method of treatment in pernicious 
anemia, found a considerable lowering of blood-pressure associated 
with increased metabolism, oxygen consumption, and loss of weight. 

The action of vanadium on different organs and tissues is but 
little understood. It appears that the intravenous injection of 
this substance in mammals is but slightly toxic to the heart. It 
causes a rise of blood-pressure due to peripheral vasoconstriction, 
but repeated injections cause a fall of pressure due to fatigue of 
the vasomotor centre and the heart. The action of moderate doses 
upon the peripheral vessels is more marked than in the case of 
barium, and upon the splanchnic vessels, more marked than 
adrenalin. 1 

Prolonged application of the x-rays to the adrenals of dogs pro- 
duces well-marked structural degenerative changes in the glands. 2 
Zimmera and Cottenot 3 obtained a prolonged clinical fall of pressure 
(20-80 mm.), associated with subjective improvement, in sixteen 
r.iMs of chronic hypertension. Quadrone reports somewhat similar 
results, but Groedel was unable to obtain any reduction in cases 
of hypertension by this means. 4 Sergent and Cottenot 8 noted a 
pressure reduction of from 40 to 50 mm. in hypertension without 
urinary abnormalities. Patients with albuminuria and those with 
marked arteriosclerosis were but little affected. There is no rational 
basis for this form of treatment. The evidence at hand is not in 



'Jackson, I). E.: The Pharmacological Action of Vanadium, .lour. Pharm. and 
Expcr. Therap., 1912, iii, 477. 

'Cottenot, Mulow et Zimmern: Action des vagons sur la corticate but renali, 
Compt. rend, hebdom. dee sciences Soc. biol., 1912, lxxiii, 717. Similar results by 
Galanaino and Decostello. 

3 La radiotherapie des glandes sur renales, ses resultats, ses effects hypotenseurs, 
Ar.h. d'electr., 1912, xx, 500. 

•Groedel, 1'.: Strahlentherapie II, 1913, p. 224. 

1 [/irradiation des glandes surrenales dans la therapeutique do 1'hypertension 
artcricllc, Hull, ci mem. Soc. Med. d. hop., Paris, 1914, xxxvii, 385. 



SURGICAL TREATMENT 335 

favor of adrenalinemia as a cause of chronic hypertension, and too 
prolonged exposure may do serious structural damage to 1 he glands. 

The usual result of exposure in a nullum emanatorium i a fall 
of the systolic blood-pressure amounting to 20 to 25 mm. Hg. 
Together with this there generally occurs a decrease in cardiac 
work and a lowering of the diastolic pressure. These changes are 
apparently due to vascular dilatation. 1 

Surgical Treatment. — Renal decapsulation lias been performed in 
some cases of chronic nephritis. Goodman reports such a case 
in which both the systolic and the diastolic pressures were very 
definitely reduced for about two weeks following decapsulation, 
although the patient ultimately died.' 

1 Loewy ami Plesch, quoted l>.\ Rowntree and Baetjer: Radium in [nternal Medi- 
cine, Jour. Am. Med. Assn., I'M.;. I\i. L438. 

- Goodman, K. II.: KITrci on 151 i-i.n--.iirc of Decapsulation of the Kidney, 

N.u \ ork Med. Jour., October 3, 1914. 



CHAPTER XIV. 

EFFECTS OF DRUGS AND GLANDULAR EXTRACTS 

ON BLOOD-PRESSURE (ARRANGED 

ALPHABETICALLY). 

Aconite. The effect of aconitin upon the mammalian heart 
may be divided into two phases: (1) It produces slowing of the 
rate with a weakening of contraction. The pulse rate may (experi- 
mentally) be reduced one-half and blood-pressure will fall propor- 
tionately. These phenomena are due to central stimulation of 
the pneumogastric nerve. (2) If the administration of the drug is 
pushed still further, tachycardia and arrhythmia appear, apparently 
;i^ a result of direct action upon the myocardium. 

Aconite has been used for the reduction of arterial hypertension, 
but its use has not been satisfactory. The tincture which is marketed 
without physiological standardization varies greatly in potency, 
and in the doses usually employed is often inert. Robinson's 1 
investigations indicate that in maximal dosage aconite increased 
ventricular irritability. 

Alcohol. There is much difference of opinion as to the clinical 
effects of alcohol on the circulation, and equally discordant findings 
have resulted from its employment experimentally. Most of the 
evidence shows that alcohol is only a momentary cardiac stimulant 
which acts reflexly through its irritation of the mouth, esophagus, 
and stomach. Its main effect is vasodilation, and if pushed, nervous 
and muscular cardiac debility. If, therefore, temporary stimula- 
tion is desired it should be given in concentrated form; if vascular 
relaxation, diluted. Although it may briefly raise the systolic 
pressure it raises the diastolic pressure even more, and thus lowers 
the pulse-pressure. 2 In chilliness due to peripheral vasoconstric- 
tion it does good, but if the patient be cold as the result of collapse, 
with a low blood-pressure, it is directly contra-indicated. It may 
act in part as a food by sparing the proteids or assist in preventing 

1 An Investigation <>f the Potency of Tincture "f Aconite, Arch. Int. Med., 1915, 
xv, Pari I. f,i:,. 

Lieb, C. C: Reflex Effects of Alcohol on the Circulation, Jour. Am. Med. Assn., 
1915, Ixiv, B98. 



ITROPIh 337 

acidosis, but in the vascular failure of infectious disea e or in 
surgical shock it is harmful. Ir is irritant to the kidneys and delays 
tlir el in i ina i ion of certain substances I uric acid, etc. I. Both clinical 
iiikI experimental evidence arc against its use as a stimulant in 
conditions of low blood-pressure. 

It produces an unstable vascular tonus. Luzzato, on admin- 
istering 30 to 50 gm. of alcohol to students, found no con tant 
relation between psychic phenomena, pulse or respiration and 
blood-pressure. 1 Sphygmobolometric studies in fever cases gener- 
ally show a diminished amplitude, a lowered pressure, and decrease 
in cardiac work.- The "/>*< t of drunkenness is associated with a 
fall of the systolic and the pulse-pressure, together with an increased 

pulse rate. 3 

The syndrome of cardiac dilatation with hypertension which is 
seen in excessive beer drinkers is in part due to the alcohol, in part 
to the increased volume of tin- blood. For obvious reasons alcohol 
should be taken sparingly if at all in case- of nephritic h\ pertension. 

Alkalies. This class of drugs may indirectly assist in lowering 
tension by counteracting acid irritant-, bj combating dyspeptic 
tendencies or by their diuretic elicit. 

Ammonium. Ammonium in the form of the aromatic spirit is 
a promptly acting though temporary cardiac stimulant. It is 
useful in transient cardiac and vasomotor weakness, and extremely 
valuable in the relief of gaseous gastric distention in arteriosclerotic 
cases with precordial oppression. The following formula ha- often 
proved most satisfactory : 

1$ — Spt. ammonii aromat ll\xxx (2.0) 

Spt. chloroformi .... TRxv L.O 

Spt. lavendulse Ttlxxx (2.0) 

Aq. menth. piperita ad f oij (8.0) 

To this prescription spirit of glonoin may sometimes be advan- 
tageously added. 

Atropin. — Atropin increases the pulse rate by depression of the 
peripheral ends of the vagus nerve. It has thus in part an antago- 
nistic action to digitalis. Experimentally it increases blood-pressure 
by a slight stimulation of the vasoconstrictor centre and an increased 
pulse rate. Clinically, pressor effects are rarely demonstrable, 

1 Luzzato: Acad, dei Fisiocritici di Siena, January 31, 1909. 

2 Dennig, Hindelang, and Griinbaum: Ueber d. Einfluss des alkohols auf d. Blut- 
druck u. d. Herzarbeit in path. Zustanden namentlich beim Fieber, Deutsch. Arch, 
f. klin. Med., 1909, xevi, 153. 

3 Holzmann: Blutdruck bei Alkoholberauschten, Arch. f. Psychiatrie, 1909, xiv, 92. 

22 



33S EFFECTS OF DRUGS ON BLOOD-PRESSURE 

although it is a valuable remedy in the wet, clammy stage of vascu- 
lar collapse, in pulmonary edema (in association with morphin), 
and in the treatment of hyperchlorhydria, which is a common 
symptom in cases of arterial hypertension. The following formula 
lias often been prescribed with benefit for the last-named condition: 

1$ — Ext. belladonna gr. A 

Pulv. rhei gr. 2 

Magnesii ustse gr. iv 

< 'arl><> litrtii gr. j. 

To be taken in capsules or as a powder after meals. 

Caffein. Caffein stimulates the entire nervous system, and 
may therefore be used if the circulatory disturbance is central in 
origin. 

Experimental Data. — Caffein injections in dogs cause a short rise 
five seconds) followed by a fall of pressure (fifteen seconds). The 
larger the dose the greater the subsequent fall. 1 Caffein raises 
blood-pressure which has been depressed by alcohol, chloral, and 
infections even in late stages. Moderate dosage is more effective 
than large doses, the latter may induce arrhythmia, palpitation, 
insomnia and gastric disturbances. Caffein increases splanchnic 
tone. The experimental data are for the most part inapplicable 
to clinical work on account of the large dosage employed. 

The rise of pressure produced by caffein, which is never great, 
is due in part to increased splanchnic tonus and in the latter stages 
also to the increased pulse rate. Owing to splanchnic constriction 
the right heart receives more blood, and as the result of peripheral 
dilatation the outflow from the left heart is increased. Furthermore, 
dilatation of the coronary arteries leads to better cardiac nutrition 2 
and more forcible contraction. The pulse rate is usually not much 
affected, but retardation is more frequent than acceleration. 3 
Large doses cause a fall of blood-pressure with diminished cardiac 
tonus. 

Caffein exerts a selective action on the vessels of the kidney. 
A primary constriction is followed by a marked secondary dilatation 
which, with a constant arterial pressure, causes a marked increase 
in local blood flow and of urinary secretion. Caffein is capable 
of increasing urinary secretion even if a volumetric increase is 
prevented, probably as the result of increased blood flow. 4 

1 Pilcher, .1. D.: Jour. Phar. and Exp. Therap., 1912, iii, 609. 

2 Meyer and Gottlieb: Die Experim. Pharmakologie, Vienna, 1910, p. 263. 
* Wood, II. C, Jr.: Therap. Gas., January 1.",, 11(12. 

1 Weber: Arch. f. exp. Path. u. Phar., 1906, liv, 1. 



THE DIGIT [LIS 'GROUP 339 

In two norm nl individuals during rest, caffein appeared to increa e 
the total blood flow and volume per beat. 1 

Clinical Data. — The effect of caffein is •<■ prompl and more 

brief than that of the digitalis group, bu1 it hu-ks the tonic effecl 
of the latter. It may be administered cither in its pure form or as 
the citrate or in the form of tea or coffee. Therapeutically it rarelj 
produces a demonstrable rise of blood-pressure. It is useful as a 
cardiovascular and renal stimulant in both acute and chronic dis- 
ease, but to be effectual must often be given in larger dosage than 
is customary. Better results are obtained by using theobromin- 
salicylate, since the untoward effects of caffein are avoided. 2 

Camphor. Camphor is said to raise blood-pressure by medullary 
and cardiac stimulation. The drug has long been used, especially 
as a cardiac stimulant. Both clinically and experimentally it 
produces at least a temporary improvement of the pulse even in 
the agonal stage of infectious disease. It is normally neutralized 
in the body and thus rendered inert by glycuronic acid, and may 
produce toxic symptoms in cases in which the latter substance is 
diminished (starvation, cachexia, sepsis, eclampsia, CO.. poisoning). 
Nothing short of a toxic dose has any effect on blood-pressure 
in normal animals because compensatory vascular changes readily 
neutralize abnormal stimuli. Head and Brooks 3 failed to get any 
definite circulatory results either clinically or experimentally. 
When applied to the isolated dog's heart no distinct or constant 
stimulation is observed 1 nor does the therapeutic dose have any 
effect upon the vasomotor centre. 5 The administration of the drug 
in emulsion has been commended as being a more certain and 
satisfactory method of obtaining the physiological effects. 6 

The Digitalis Group. — Based purely upon experimental evidence 
digitalis should be the ideal drug to employ in case of arterial 
hypotension, since it increases the force of cardiac contraction as 
well as vascular tonus. Clinical data, however, show that in 
therapeutic dose digitalis often does not increase blood-pressure; 
in fact, it frequently lowers it, especially in heart diseases with high- 
pressure stasis and in hypertension due to toxic renal retention. 
If prompt action is desired it should be given intravenously (digi- 
folin, digipuratum, strophanthin, ouabain). If given by mouth 

1 Means and Newburgh: Tr. Assn. Am. Phys., 1915, xxx, 51. 

2 Taylor, L: Clinical Studies in Caffein, Arch. Int. Med., 1914, xiv, 769. 

3 Am. Jour. Med. Sc, 1913, cxlv, 238 (bibliography). 

4 Plant, O. H.: Jour. Phar. and Exp. Therap., 1914, v, 571. 
6 Pilcher and Sollmann: Jour. Exp. Med., xxi, 330. 

6 Doetorrwitch: Therap. d. Gegenw., xlvii, 343. 



340 EFFECTS OF DRUGS ON BLOOD-PRESSVRK 

its effects are not evident for twenty-four hours or more. There 
has been much discussion regarding its effect upon the toxic heart 
of fevers, many authorities maintaining its uselessness in pneumonia, 
typhoid fever, etc. Important evidence of its activity has been 
furnished by Cohn, 1 who showed electrocardiographically, although 
the heart-rate remained unaffected, other digitalis effects — pro- 
longation of the a-c interval and inversion of the T-wavc were 
produced in hearts with a normal sinus rhythm, while the same 
rate changes were noted in cases of auricular fibrillation or flutter 
as occurred in afebrile oases. II. ('. Wood, Jr., believes that although 
medicinal doses of digitalis do not raise blood-pressure, yet they 
probably do have some slight effect on the vasomotor system. This 
view is based upon the fact that: (1) if slowing of the pulse is 
abolished by atropin, strophanthus causes a marked increase of 
pressure in normal man; (2) the diuretic effects of the drug, 
although independent of systemic pressure changes, may result 
from a relative splanchnic contraction at a time when the renal 
vessels are dilated by the drug. 2 

Marvin, 3 in experiments on healthy students, found an increase 
in blood-pressure (average 13 mm.) which reached its maximum in 
five hours and gradually returned to the normal in fifty hours. 

Digitalis is the most useful drug in cases of hypertension when 
the heart is beginning to fail. In such cases its use need not be feared 
on account of increasing vascular pressure. This effect is generally 
not in evidence, whereas it often lowers tension, especially the 
diastolic pressure, by securing better elimination and a more efficient 
circulation. In auricular fibrillation digitalis does raise the average 
systolic pressure (see page 251). The action of digitalis and digi- 
toxin is more prolonged than that of strophanthus and digitalin. 4 

In nephritic hypertension, as the renal lesion progresses, pressure 
continues to rise, and unless some other lethal termination occurs, 
either the heart or the vascular system must in time give way. 

Heart failure may manifest itself by (1) a fall of blood-pressure, 
edema, dyspnea, oliguria, and cardiac dilatation, or (2) high-pressure 
stasis, a condition in which blood-pressure remains high or even 
rises (increased toxemia) and is associated with dyspnea, cardiac 
arrhythmia and visceral stasis. 

In both these conditions digitalis is indicated, but especially if 
the systolic and diastolic pressures are low, and the pulse-pressure 

ohn, A ]■;.: Digitalis in Pneumonia, Jour. Exper. Mod., 1917, xxv, 65. 
\\ ood, EL C, Jr.: Newer Ideas Concerning Digitalis, Therap. Gaz., Juno 15, 1915. 
Vrch. Int. Med., 1913, ri, lis. 
4 Hatcher, H. A.: The Persistence of Action of the Digitalins, Arch. Int. Med., 
1912, x. 268. 



//// DIGITALIS GROt P 3 ll 

small. In these cases digitalis often increases the pulse-pressure 
and improvement occurs. Under its administration renal elimina- 
tion is increased and, in high-pressure eases, an actual lowering 
of arterial pressure is not infrequently seen. The final break can 
often be delayed by appropriate stimulation, for which purpose 
digitalis is by far the most satisfactory remedy. 

Digitalis exerts its effects on the kidney indirectly bj its local 
effect on blood flow; it also produces a direct local dilatation of 
the renal vessels. Its chief use in renal disease consists in its 
improvement of the local circulation by its effed upon the heart. 
Experimentally, ligation of the renal vein causes suppression of 
urine as well as ligation of the renal artery, showing thai secretion 
is a question of blood How, not merely of blood-pressure, and digi- 
talis not only increases arterial How bu1 diminishes venous stasis. 
When too freely administered, digitalis may cause centric cnmit'.uij. 
It has long been taught that emetics should not he given to arterio- 
sclerotics lest the increased blood-pressure produced cause vascular 
rupture. 

From recent researches' it appears that vomiting is generally 
associated with a sudden and very great fall of pressure, due to 
cardiac inhibition but always associated with very great pressure 
variations. Great and sudden pressure oscillations may cause 
vascular damage at actual pressure heights which, hid the rise been 
gradual, would have been without serious effect. It is jusl as 
important, therefore, to avoid emesis in arteriosclerosis as was 
early taught, though for a somewhat different reason. 

Failing cardiac compensation is frequently associated with an 
increase of venous blood-pressure to or above 20 em. Such a rise 
is therefore prognostically unfavorable, especially if it continues or 
increases despite the administration of digitalis or its congeners. 2 

Strophanthus and squills act in the same manner, but are less 
satisfactory than digitalis because of the variability of absorption 
of the former and because of the variability of activity and irritant 
(gastro-intestinal) qualities of the latter. In therapeutic dose 
neither strophanthin nor digalen affect the volume of the arm nor 
its normal reaction to the application of cold, although injections 
of these substances are said to affect the tonus of the larger arteries. 3 

1 Brooks, C, and Luckhardt, A. B.: Blood-pressure during Vomiting, Am. Jour. 
Physiol., 1915, xxxvi, 104. 

2 Clark, A. EL: The Diagnostic and Prognostic Significance of Venous Pressure 
Observations in Cardiac Disease, Arch. Int. Med., 1915, xvi, 5S7. 

3 Hewlett, A. W.: The Circulation in the Arm of Man, Am. Jour. Med. Sc, 
1913, cxlv, 656. 



342 EFFECTS OF DRUGS 0A r BLOOD-PRESSURE 

Depressants.— Chloral, the coal-tar group, bromides, etc., will 
in sufficient dose lower blood-pressure. They should, however, 
never be used for this purpose, although they may on occasion be 
useful in relieving pain or promoting sleep. Chloral may produce 
degenerative changes in heart and liver similar to those following 
the administration of chloroform. 

Emetin. — This drug is sometimes administered intravenously. 
This is not a safe procedure, since the drug is a cardiac depressant. 
If this method of administration must be employed, coincident 
blood-pressure readings are desirable with a view of detecting 
evidences of circulatory failure (R. L. Levy). 

Epinephrin. - (See under Physiology, page 35.) Epinephrin may 
be administered by mouth without any demonstrable cardio- 
vascular action. Prolonged use in this way leads to dyspepsia 
associated with colicky pains. Large doses given to rabbits produce 
arterial degeneration without increasing blood-pressure. 

Experimental Data. Epinephrin produces upon the cardio- 
vascular system the same effect as would electric stimulation of 
the sympathetic — a marked rise of blood-pressure due to vaso- 
constriction and increased cardiac action (increased systolic output). 
This rise is of brief duration, due to fatigue. Venous pressure 
rises slightly. The different arteries are contracted in proportion 
to their sympathetic innervation. The coronary arteries are said 
to be unaffected (Schafer), owing to the absence of sympathetic 
fibers. In experimental animals epinephrin causes coronary dila- 
tation, but in man (isolated arteries) and in monkey (perfused 
hearts) it causes coronary constriction, presumably because in the 
latter species the arteries are supplied with constrictor nerves 
of true sympathetic (thoracicolumbar) origin. 1 Epinephrin dimin- 
ishes the pulse rate through vagus stimulation. 2 In small dose it 
increases the rapidity of the pulmonary circulation; in excessive 
dose it may cause pulmonary edema in men (Bennett) as it does in 
animals. Large doses and vagus stimulation diminish it. Apnea 
during artificial respiration has no effect on pulmonary circulation. 3 
The intraspinal injection of adrenalin causes a slower but more 
prolonged rise of pressure (40 mm. for half an hour or longer), 

1 Barbour and Prince: Influence of Epinephrin on the Coronary Circulation of th; 
Monkey, Jour. Exp. Med., 1915, xxi, 300. 

- Meek and Eyster: Effect of Epinephrin on the Heart Rate, Am. Jour. Physiol., 
I'M.",, xxxviii, No. 1. 

ois, 1'., and Desbouis, G.: Sur La vitesse de la circulation pulmonaire, 
Adrenaline, Digitaline, Asphyxie. Respiration Artificielle, Mora. 2, Jour, de physiol. 
et de PathoL gen., 1012, xiv, S. 1113-1123. 



EPINEPHBIN 343 

although occasionally preceded by a primary fall (!) to 51 I mm. 
for a half to four minutes). 1 

In using intraspinal injections care must be taken to avoid 
sudden increase of pressure. It is safer to allow inflow only by the 
force of gravity. Too high an intraspinal pressure is firsl mani- 
fested by cessation of respiration, soon followed by cardiac inhibi- 
tion and an enormous fall of Mood-pressure. To combat cardiac 
failure under these circumstances atropin is the most useful drug, 
whereas cocain is the best respiratory stimulant. Since the fall 
of pressure is not due to vasomotor failure, epinephrin is not 
indicated. The lowering of the intraspinal pressure after symptoms 
have arisen is unproductive of benefit. It has been -suggested thai 
a local hypodermic prophylactic injection of cocain and atropin be 
given at the site of the spinal injection, especially if the patienl 
be under the effects of chloroform, since it ao1 only minimizes the 
danger of sudden death but allows a larger injection to be given 
(Carter). 2 (See page 410.) Experimentally, epinephrin has by some 
investigators been found to be beneficial in hemorrhage, chloroform 
poisoning, pneumococcus septicemia, and diphtheria intoxication. 
On the other hand, Gottleib has shown that in rabbits receiving 
diphtheria toxin daily until cardiovascular symptoms appear, the 
injection of adrenalin only produces a brief and deceptive rise of 
arterial tension which soon leads to a fatal termination. 3 

Epinephrin is very rapidly effective in its pressor effect when 
intratracheally injected. Absorption appears to occur by the capil- 
lary route into the pulmonary veins and is quickly manifest, even 
in pulmonary edema, although absorption is in this condition 
greatly handicapped. 4 

Clinical Data. — A marked fall of blood-pressure due to vaso- 
motor depression without cardiac weakness is the chief indication 
of the use of epinephrin. Thus in shock, chloral poisoning, and 
collapse occurring in ether or chloroform narcosis it is decidedly 
useful. It should be administered intravenously in 5- to 10-minim 
doses (1 to 1000 solution) or, better still, in the proportions of 1 to 
50,000 as a continuous saline infusion. If a slower and more pro- 
longed action is desired it may be given subcutaneously, in which 
event its effects are usually manifest in from five to fifteen minutes. 

1 Auer and Meltzer: Proc. Soc. Exp. Biol, and Med., 1912, ix, 79. (Experiments 
on deeply narcotized apes.) 

2 The Effect of Intraspinal Injections of Ringer's Solution in Different Amounts 
under Varying Pressures, Arch. Int. Med., 1912, x, 425. 

3 Gottleib: Arch. f. exp. Pharm., xxxviii and xliii. 

4 Auer, J., and Gates, F. L. : The Absorption of Adrenalin after Intratracheal 
Injection, Jour. Exper. Med., 1916, xxiii, 757. 



344 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

One naturally thinks of epinephrin in the vasomotor paresea 
<tf infections, but its use is under these circumstances disappointing. 
The condition here is not a sudden emergency with a good cardiac 
muscle, bu1 a gradual failure of vasomotor and often cardiac 
strength. We must not forget that if the heart weakness is present 
a sudden increase of arterial pressure may he more of a load than 
the staggering organ can hear. The best and most lasting effects 
are obtained by slow intravenous administration in dilution with 
normal salt solution. Epinephrin has proved useful in vasomotor 
failure due to diphtheria, pneumonia, plague, peritonitis, and in 
surgical shock. 

Hypodermic epinephrin injections are variable in their effects. 
They do not always increase hlood-pressure, but when they do so 
the rise generally lasts about one hour. The systolic phase is 
influenced more than the diastolic, indeed the latter may actually 
fall. Glycosuria may occur, but this bears no constant relation to 
pressure changes. A preliminary dose of atropin may increase the 
reaction even without increasing the heart rate. Marked reactions, 
both objective' and subjective, are often produced in cases of essen- 
tial hypotension, whereas low pressure due to diarrhea and cachexia 
is but little influenced by epinephrin. In arterial hypertension 
marked reactions are sometimes obtained and caution must be 
observed. Epinephrin increases the demarcation of the sound 
phases as heard in the auscultatory estimation of blood-pressure 
(Clough). 

Fresh preparations of epinephrin must be employed, since old 
preparations loose their constrictor but not their depressor effect, 
and hence an intravenous or intramuscular dose may actually 
lower blood-pressure. 

Ergot. Experimental Data. — " The action of ergot may be shortly 
defined as a primary stimulation followed by paralysis (if given in 
large dose) of the motor terminations of the sympathetic nerve, 
which arises from the thoracic and lumbar spinal cord. The point 
at which ergot acts is thus analogous to that affected by adrenalin, 
but the range of ergot is more limited, for adrenalin affects not 
only the motor or positive nerve ends but also the inhibitory or 
negative fibers. In addition the effects of ergot are not so transitory 
as those of adrenalin, while, on the other hand, the latter does 

not exercise any subsequent paralyzing action of consequence" 
(< lushny I. 

An intravenous injection of ergotoxin is followed by a prompt, 
abrupt /-/.st of bloodr^pressure; this occurs after section of the 



HYDRASTIS 345 

splanchnic nerves, showing it to be a peripheral effect. The vessels 
of the abdomen and the extremities become contracted. The pulse 
rate is often i ne reused at first, then diminished pan I \ Prom tbe vagus 
stimulation from high bloods-pressure and partly from direel action 
upon the heart muscle. The rise of pressure varies greatlj in 
different species (Cushny). The administration of a large dose 

produces a secondary fall of arterial tension due to paralysis of 

the sympathetic fibers, which even epinephrin fails to overcome. 1 

Para-oxyphenylethylamin (isolated from ergot). Experimentally 
this substance causes a rise of pressure due to capillary conl rad ion 
associated with bradycardia and an increased pulse amplitude and 
diminution of blood in the veins. Its action is transient and 
followed by normal readings. 2 

Clinical Data. Ergol is of very little if any use as a drug with 
which to restore vasomotor tone, its effects being verj fugacious. 
Its action upon the pulmonarj circulation has been discussed under 
Hemoptysis (see page 226). It is highly important that all ergot 
preparations used in medicine be physiologically standardized, 
not only because some preparations are inert bu1 also because it 
has been shown that ergot sometimes contains -mall amounts 
of acetylcholin which has been pronounced to he the most powerful 
circulatory depressant known, as small an amount as one-millionth 
part of a milligram causing a fall of hlood-pressiire in rabbits. 3 

Hydrastis. — Although rarely employed in medicine, hydrastis is 
occasionally recommended in the treat m cut of hemoptysis owing 
to a supposed vasoconstrictor action. Experimental evidence, how- 
ever, indicates that it has no such effect. W. W. \Yilliams, 4 from 
a careful experimental research, comes to the following conclusions: 

The most constant and conspicuous effect of the intravenous 
injection of hydrastis is a prompt fall of blood-pressure. With 
small doses the pressure promptly returns to normal, and there 
may be a slight rise above normal. With larger doses from (0.07 c.c. 
to 1 c.c. per kilogram of body weight) there is only partial recovery 
from the fall of blood-pressure, or it may remain low. The pressure 
phenomena are attributable to depression of the cardiac muscle, 
causing the fall, and to stimulation of the muscle, causing the rise. 
Very large doses depress and paralyze the vagus and vasomotor 

1 Dale: Jour. Physiol., 1906, xxxiv, 163. 

2 Bickel, A., and Pawlow, M.: Untersuchungen z. pharm. Wirkung des p. Oxy- 
phenylaethylamins, Biochem. Ztschr., 1912, xlvii, 345. 

3 Editorial, Jour. Am. Med. Assn., 1914, lxiii, 2136. Discussion and literature. 

4 The Effects of Hydrastis and its Alkaloids on Blood-pressure, Jour. Am. Med. 
Assn., January 4, 1908, p. 26 (bibliography). 



346 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

ii ; otherwise there is no evidence deduced from the myo- 
cardiograins and oncometer that the vasomotor system has any 
Important part in the blood-pressure changes. 

The two principal alkaloids of hydrastis, hydrastin and berberin, 
cause qualitatively the same blood-pressure changes, although 
In rberin is the more active and is responsible for about 85 per cent. 
of the effect of hydrastis— hydrastin causing the remaining 15 per 
cent. Hydrastis given by mouth or hypodermically causes no 
change in the blood-pressure, heart rate, or respiration. 

Hydrastinin, an artificial alkaloid, derived from hydrastin, causes 
a rise of blood-pressure above normal, which is usually preceded by 
a slight fall when injected intravenously. The rise is well sustained 
and is principally caused by stimulation of the cardiac muscle. 

"The results of this investigation do not support the clinical 
theories concerning hydrastis. It is possible that conditions in 
man and in disease may modify the actions observed by me, but 
this is rather improbable. At least the uniform contradiction of 
the experimental results and clinical opinions demands that the 
latter be examined critically before they are accepted." 

Hormonal.— This drug has been used as a remedy against intes- 
tinal atony and paralysis. Mohr states that his experimental 
research on hormonal has established beyond question its pro- 
nounced effect in reducing blood-pressure even with doses propor- 
tionately far below those used in the clinic to date. He had an 
experience with a threatened collapse in a man, aged twenty-eight 
years, after intravenous injection of 14 c.c. of hormonal, and since 
then, he says, four similar cases have been reported. Madlener has 
recently reported the death of a patient after injection of 20 c.c. 
hormonal for paralytic ileus following a myoma operation. Saba- 
towski's research on dogs has further confirmed the sudden pro- 
nounced drop in the blood-pressure after intravenous injection of 

hormonal. 

The Iodides.— There is a difference of opinion regarding the effect 
of the iodides on blood-pressure. Certainly they are not active vaso- 
dilators in the sense that the nitrites are. On the other hand, cases 
are occasionally encountered in which a lowering of tension occurs, 
a response which naturally suggests that the hypertension was 
reflexly due to syphilitic aortitis or directly to endarteritis. The 
former maj exerl an effeel od the depressor nerve, the latter may 
cause Ins, of vascular elasticity from cellular infiltration. 

Experimentally, potassium iodide, if administered intravenously 
causes a fall of blood-pressure, but it has been shown that this 



THE VITRITE GROX P 



347 



effect is solely due to the effect of the kation (potassium) while 
the action of the ion (iodide) is actually one of stimulation, both 
of heart and bloodvessels. 1 

The absorption of iodides horn the intestinal trad i rapid up to 
a certain point, beyond which a stoppage occurs which apparently 
results from some local action. It is unaffected by blood-pre are 
except when this is very low, when absorption is somewhal slower. 2 

So far as hypotensive effects arc concerned, the iodides maj be 
employed in syphilitic arteritis and in lead poisoning, q. v. The 
custom of giving small doses over prolonged periods of time in other 
varieties of hypertension, while \ci\ common, is probably useless. 
The iodides have no direct effed upon blood-pressure. 

Mistletoe (Viscum Album). Mistletoe has been used, chiefly 
in Europe, for the purpose of lowering blood-pressure. Experi- 
mentally (in a dog) intravenous injection promptly and progres- 
sively lowers blood-pressure 20 to 30 nun. ETg. This is associated 
with acceleration of the pulse, with diminished amplitude, and 
after a stationary period, a gradual rise of pressure to the uormal 
level (one to two hours). This action is the result of central depres- 
sion of the vasomotor centre. 3 Mistletoe has been given in doses of 
30 to GO m. of the fluidextract, and as guipsine, a glucoside which is 
said to represent the active properties of the drug. This is given in 
pill form in doses of 5 cgm., three or four times daily. 1 




Fig. 102. — Diagram showing the comparative promptness of action and duration of 
effect of different blood-pressure-lowering drugs. (After Mathews.) 

The Nitrite Group. — The most potent, as well as the most mal- 
administered and abused of the blood-pressure-lowering remedies are 
the nitrites. Their action is rapid and their effect is for the most 



1 Macht, D. I.: Action of Potassium and Sodium Iodides and of Iodine Ion on the 
Heart and Bloodvessels, Bull. Johns Hopkins Hosp., September, 1914. 

2 Hanzlik, P. J. : Quantitative Studies on the Gastro-intestinal Absorption of 
Drugs, Jour. Pharm. and Exp. Therap., 1912, iii, No. 4. 

3 Gaulthier, R. : Etudes physiologiques sur le qui, Arch. Internat. d. pharmaco- 
dynamic, 1910, Nos. 1 and 2. 

4 Williamson, O. K.: Observations on the Use of Guipsin as an Apressor Remedy 
in Cases of High Arterial Blood-pressure, Practitioner, May 11, 1911. 



34S EFFECTS OF DRUGS ON BLOOD-PRESSVRE 

part fugacious. Furthermore, a tolerance for this class of drugs is 
rapidly established (Fig. 102). They should therefore be given fre- 
quently and in sufficient dose to produce their physiological effect. 
The typical action is not only vasodilatation but also an increased 
systolic output which occasions a more rapid How. 1 The following 
table shows the effect of these drugs upon normal individuals: 

Average Blood-pressure Results from Administration of Nitroglycerin, 

Sodicm Nitrite, and Erythrol Tetranitrate to Normal Persons. 

(Wallace and Ringer.) 

Time of Time of Time of Maximum 

beginning maximum duration of extent of 

action. effect. action. action. 

Drug. Min. Min. Min. Mm. Hg. Percent. 

Amy] nitrite. :\ minima .1 3 7 15 11 
Nitroglycerin, l", minims, 

1 per cent. sol. ... 2 8 30 15 11 

Sodium nitrite, 1 gr. . . 10 25 60 14 13 

Erythrol tetranitrate, j gr. 15 32 120 to 240 16 14 

It will be noted that promptness of action and duration of the 
effect will tend to vary inversely. The therapeutic effects are 
obtained about as promptly when the drug is given by mouth as 
when it is administered hypodermically. The percentage of fall 
is markedly uniform, the higher the initial pressure the greater 
the drop. 

It is important to remember not only that tolerance to the nitrites 
is often quickly established but also that the effect of different 
members of the nitrite group may vary in their effect upon a given 
individual. 

Physiological Ad ion. — Different members of the nitrite group of 
drugs have an essentially similar action. Their effects vary only 
in promptness, intensity, and duration. The chief action of the 
nitrites is tjiat of lowering blood-pressure (depression of the nerve 
endings and musculature of the arterioles) and acceleration of the 
pulse rate, thus causing an increased rate of blood flow. The veins 
are also dilated. The vessels most affected are those of the 
splanchnic system and of the head. The vasomotor centre is not 
depressed but as a rule actually stimulated, 2 probably as a result of 
medullary anemia. The nitrites are believed to cause constriction 
of the pulmonary arteries, since local application causes a con- 
traction of arterial strips.' 5 Such an action would render their 
employment in pulmonary edema rational. 

'Cameron and Hewlett: .lour. Med. Research, December, 1906. 
•• Richer and Sollman: .lour. Phar. and Exp. Therap., vi, 323. 
Mi< lii : Jour. Phar, and Exp. Therap., vi, 13. 



THE VITRITE GROUP 349 

Mode of Acinm. Nitroglycerin is represented by the formula: 

CH.ONO2 
CHONO2 
CH2ONO2 

"It is probable, however, that in the presence of water and 
hydrochloric acid in the stomach it is decomposed, and thai its 
decomposition products NO2 and NO arc disengaged in the form 
of brown vapors which arc irritants and strong oxidizers. These 
ultimately produce an impression on the centripetal nerve endings 
in the gastric mucosa, which impulse is carried to the vasomotor 
centre and by the centrifugal nerves conveyed from the centre 
of the vascular wall, thereby causing the expansion of the vessels. 
This dilatation is due either to inhibition of the vasoconstrictors 
or to stimulation of the vasodilators" (W. II. Porter). 1 

Not infrequently patients exhibit marked idiosyncrasies to the 
nitrites: some bear them very badly and are much more affected 
by one member of the nitrite group than by another; others can 
take enormous doses (one grain of nitroglycerin daily has been 
given with apparent benefit). The administration of the nitrites 
coincidently with digitalis is a therapeutic blunder. The effect of 
the former will have passed off long before that of the latter has 
begun to act. Nitroglycerin has a retarding effeel on renal secretion 
(Loeb). Nitrite of amyl acts primarily upon the cerebral vessels — 
more so than the other nitrites. 

Average Blood-pressure Results from Administration of Nitroglycerin, 

Sodium Nitrite, and Erythrol Tetranitrate to Patients with 

Arteriosclerosis. (Wallace and Ringer.) 2 



Drug. 


Time of 

beginning 

action. 

Min. 


Time of 
maximum 

effect. 
Min. 


Time of 
duration 
of action. 

Min. 


Minimum 
extent of 

action. 
Mm. Hg. 


Per cent. 


Nitroglycerin, ^g gr. 


2 


8 


35 


32 


17 


Sodium nitrite, 2 gr. 


. . 15 


45 


120 


53 


25 


Erythrol tetranitrate, 


2 gr. 30 


60 


180 


60 


30 



In hypertensive cases the response is sometimes less prompt 
(delayed absorption) and the action more prolonged (delayed excre- 
tion). The percentage fall is much the same in both tables. Head- 
ache is less frequent in high-pressure cases; indeed, it is often 
relieved by these drugs. 

1 Jour. Am. Med. Assn., August 3, 1912. 

2 The Lowering of Blood-pressure by the Nitrite Group, Jour. Am. Med. Assn., 
1909, liii, 1630. 



350 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

The employment of the nitrites in hypertension is purely symp- 
tomatic medication. It temporarily relieves high pressure as certain 
forms of headache are relieved by acetanilid. It does not affect 

the underlying cause, and if used indiscriminately may do actual 
harm. The nitrites are often given in too small doses and too 
infrequently, especially since toleration is rapidly established; 
- 1 ,, grain of nitroglycerin is often a better dose than T Jo, and as 
high as ,'„ may be given in emergencies. 

The nitrites are essentially emergency drugs to be given in case 
of a threatened apoplexy or cardiac failure from hypertension, 
etc. The splanchnic dilatation relieves the systemic, especially the 
intracranial pressure, but, of course, after intracerebral vascular 
rupture has occurred the nitrites are contra-indicated. Many 
preparations on the market are inert. The dosage must be based 
on the physiological effect, flushing, headache, and a fall of pressure. 
Nitroglycerin is also used as a therapeutic test agent to determine 
whether certain symptoms are due to spastic vascular contraction. 
It is contra-indicated in arterial hypotension, and should therefore 
not be used as a primary cardiac stimulant in acute febrile disease 

or shock. 

Form nf Administration.— Nitrite of avnjl, in glass capsules (to 
be kept in the dark), to be crushed in a handkerchief and inhaled. 
The primary fall of pressure is followed by a rise to above the original 
level (Hewlett) . In cases of cardiac weakness, instead of a secondary 
rise of 6 to 10 mm., a fall of pressure occurs (Abrams). 

Nitroglycerin, perferably as a 1 per cent, solution (spintus 
glycerylis nitratis), to be swallowed, or as tablets to be dissolved 
on the tongue. Dose T |o to T V grain. 

No,//,,,,, Nitrite.- Tablets or be swallowed or dissolved on the 
tongue. Dose: gr. ss to gr. ij (solutions deteriorate rapidly). 

Erythrol Tetranitrate. Tablets. Dose: gr. I to gr. ss. Erythrol 
tetraiiitrate produces the most severe headaches. 

Uannitol nitrate (gr. j); effect even more prolonged than erythrol. 
On the whole the spiritus glycerylis nitratis is the best prepa- 
ration, both because of its reliability and because of the ease with 
which the dose can be increased. ^ 

If a prolonged and gradual effect is desired the nitrites should 
be given after meals. If taken between meals the drug should be 
well diluted. Sudden effects are generally as useless as they are 
undesirable. 

Summary. 1. "The general indicatwm for the use ot mtro- 
glycerin are (a) to relieve symptoms of localized arteriosclerosis 



OPIUM 351 

or arterial spasm in vitally important regions of the body and 

when there is pain due to contracted or diseased arteries in other 
regions; (6) to reduce general high blood-pressure in selected 
eases, if its continuance threatens accidents to the cardio\ a-,riil;ir 
apparatus; and (c) to clear the diagnosis (see p. 311). 

2. "The chief contra-indications to the use of nitroglycerin are 
(a) low or relatively low blood-pressure; (6) advanced chronic 
nephritis with very high blood-pressure and toxemic conditions 
producing high blood-pressure, as a rule; and (c) the presence of 
an idiosyncrasy in regard to it- action." 1 

Opium. In some cases of hypertension (angina pectoris, broken 
compensation, etc.) morphia is an indispensable drug. It often 
produces a most satisfactory fall of pressure as well as relief from 
symptoms, the former being doubtless largely due to its general 
sedative influence on the nervous system and it- stimulation of the 
vagus nerve. Under its influence the cyanotic skin is often replaced 
by a pink Hush indicating a dilatation of the peripheral circulation. 
The danger of this drug in nephritis has been greatly overestimated. 
The beneficial effects of opium are also in part due to its effeel on 
the respiration. Edsall has shown that superficial rapid respira- 
tions such as are seen in cardiac dyspnea, etc., are functionally 
less efficient than slower labored movements. 2 It tends to lower 
blood-pressure by central vagal slowing of the pulse. 3 In tin case 
of normal hearts during nocturnal sleep the pulse rate is slowed 
about twenty beats per minute, and although the slowing thus 
produced become progressively less, the worse the cardiac com- 
pensation, yet notwithstanding the establislmient of sleep, induces 
very considerable cardiac rest. 4 Morphin produces a mild, codein 
only a slight, dilatation of the coronary arteries. Narcotin and 
papaverin cause marked dilatation. But morphin and narcotin 
combined have less effect than either separately. A combination 
of caffein (which of itself produces coronary dilatation) with papa- 
verin causes dilatation of the coronary ring. 5 

Papaverin in addition to its analgesic effect produces a slight 
slowing of cardiac rate, and increased myocardial tonicity and a 

1 Cornwell, E. E.: When and How to Use Nitroglycerin, Jour. Am. Med. Assn., 
1913, lxi, 118. 

2 Edsall, D. L.: The Efficiency and Significance of Different Forms of Respiration, 
Tr. Assn. Am. Phys., 1912, xxvii, 560.. 

3 Van Egmond: Die Wirkung des Morphins auf d. Herz, Arch. f. exp. Path., 
1911, lxv, 197. 

4 Klewitz, F.: Der Puis im Schlaf, Deutsch. Arch. f. klin. Med., 1913, cxii, 38. 

5 Macht, D. I.: Action of the Opium Alkaloids, Jour. Am. Med. Assn., 1915, 
lxiv, 1489. 



352 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

fall of blood-pressure resulting from peripheral action on the vascular 
walls. 1 These properties suggest its use in angina pectoris and 
arterial hypertension when an analgesic or sedative is required. 

In the last-named qualities its seems to be the equal of codein. 

Pilocarpin. Is a powerful diaphoretic, the physiological action of 
which is directly opposite to that of atropin. Full doses slow the 
cardiac rate and diminish contraction through vagus stimulation. 
Still larger doses depress the heart muscle directly. Toxic doses 
cause peripheral vasodilatation by depressing the vasoconstrictor 
centre. It therefore tends to lower blood-pressure. 

It lias long been used as a diaphoretic in renal disease, especially 
in conjunction with hot packs or hot-air baths if the patient does 
not sweat sufficiently from the latter procedures alone. It must, 
however, be given with caution in cases of heart weakness, since 
it may produce pulmonary edema. This accident can, however, 
be promptly corrected, if treated in time by full doses of atropin 
(gr. 3V hypodermically). The usual dose of pilocarpin for adults 
subcutaneously is tV grain (0.000). 

It has been recommended in small doses (gr. 3V) thrice daily in 
water after meals to relieve arterial hypertension and its associated 
symptoms, especially headache. 2 

Pineal Extract. — Aqueous extracts of pineal gland were found by 
Eyster and Jordan 3 and by Ott and Scott 4 to produce a slight fall 
of pressure when injected intravenously. Other investigators, 
however, have shown that the blood-pressure effects of pineal 
extract are insignificant. 5 

Pituitary Extract. — The infundibular portion of the gland has a 
more prolonged though less marked and rapid blood-pressure 
raising effect than epinephrin. Too frequently repeated it depresses 
respiration. It also has a diuretic effect due to direct stimulation 
of the renal cells, usually aided probably by a concomitant vaso- 
dilatation, because there is no constant relation between pituitrin 
diuresis and either systolic or pulse-pressure or the ratio between 
them. As a general rule, however, it is accompanied by a decreased 
pulse-pressure. 8 Furthermore, there is no constant relationship 

1 Macht, I). L: A Pharmacological and Clinical Study of Papaverin, Arch. Int. 
Med., 1916, xvii, 786. 

* Robinson, W. I).: Pilocarpin in High Blood-pressure, Tr. Am. Climat. Assn., 
1914, xxx, 200. 

I ter, .1. A. E., and Jordan, H. E.: Am. Jour. Physiol., 1010-11, xxiii, 25. 

«Ott. .!.. and Scott, J. C: Cyol. and Med. Hull., 1912, v. 207. 

&Dix<m and Halliburton: The Pineal Body, Quart. Jour. Exper. Physiol., 1909, 
ii, 282. 

•Hoskinfl and Means: Relation of Vascular Conditions to Pituitiin Diuresis, 
Jour. Phar. and Exper. Therap., 191.3, iv, No. 5. 



STROPHANTHUS 353 

between renal volume and pituitary diuresis, 1 with local renal vaso- 
dilatation. 2 It stimulates the heart bu1 in animals has no efl'ect 
upon the vasomotor centre. It stimulates intestinal peristalsis 
and is sometimes useful for tympanites. It may be given hypo- 
dermically, intravenously, or by mouth. It maj be used instead 
of epinephrin in eases of temporary hypotension or in cases of pul- 
monary hemorrhage, q. ». It causes contraction of the peripheral 
arterioles, increases cardiac contraction, and slows the pulse. These 
results are due to a direct effect upon the cardiac and arterial mus- 
culature. It lias been recommended in all cases in which lowered 
blood-pressure is due to loss of splanchnic vascular tone, and in 
hypotension due to shock or toxemia, especially in combinal ion with 
saline infusion. 3 Musser, Jr., 4 who administered pituitary extract 
by mouth (0.065 dried "'land, q. d.) obtained very constantly a 
distinct elevation of blood-pressure (up to 28 mm. Hg.) which often 
persisted for a time after discontinuance of the drug. The injection 
of 1 c.c. of pituitrin is followed within a few minutes b\ a rise of 
pressure averaging 25 to 30 mm., which lasts for about half an hour.'' 
Diarrhea was sometimes produced. Commerical preparations of 
the posterior lobe vary greatly in potency, and should be standard- 
ised, Roth suggests, by their action on the isolated uterus of the 
virgin guinea-pig. 

Spartein. — Experimentally given to dogs in doses of 5 mg. per kilo, 
spartein produces a slight initial rise of blood-pressure and an 
increased pulse rate. This increase of pressure is brief and is 
followed by a pronounced fall. In from one to three minutes 
pressure returns to normal. If the dosage is doubled a more marked 
and prolonged fall of pressure occurs. The latter dose if repeated 
often kills. 6 Spartein sulphate stimulates the vagal ganglia and 
depresses the heart muscle. It slightly stimulates the ganglia 
of the vasoconstrictor nerves but clinically produces no demon- 
strable rise of blood-pressure. 

Strophantus. — The action of this drug is essentially that of 
digitalis. Its effects are somewhat less lasting, perhaps because, 
as suggested by Eggleston, it is less firmly fixed in the tissues and 
more promptly eliminated. If used, it should be given intraven- 

1 Schaeffer and Herring: Philos. Tr. Royal Soc, Sect. B, 1908, excix, 1. 

2 King and Stoland: Am Jour. Physiol., 1913, xxxii, 405. 
3 Klotz: Internat. Congr. Physiotherapy, Berlin, 1913. 

4 Effects of Continuous Administration of the Pituitary Gland, Am. Jour. Vied. Sc, 
1913, cxlvi, 208. 

5 Arbuck, S. S., and Rongy, J. A.: New York Med. Jour., 1914, p. 878. 

6 Haskell, C. C, and Thomas, H. B.: Physiological Action of Spartein Sulphate, 
Old Dominion Jour. Med. and Surg., 1916, xxii, No. 2. 

23 



354 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

ously in the turn, of strophanthine Its absorption from the gastro- 
intestinal tract is variable and uncertain (Hatcher). 

Strophanthin and ouabain have been shown to act upon the heart 
even in febrile conditions in their characteristic digitalis-like manner, 
except that no slowing of the pulse occurs (Cohn). If the heart 
does not respond it is not because of the degree of fever, but perhaps 
owing to the presence of toxins;- indeed, it appears that ouabain 
is more prompt in its effect upon the rabbit's heart if the bodily 
temperature is raised. 

Salvarsan— Experimentally, small doses produce but slight and 
temporary effects on blood-pressure. Moderate doses cause a slight 
fall at the end of two minutes, a secondary rise and a tertiary 
decline (two to six minutes). Large doses lower pressure at once. 
Both alkaline and acid solutions of salvarsan experimentally cause 
a fall of blood-pressure. If an excess of alkali is added blood- 
pressure may rise but this is purely due to the alkali which has 
physiologically overantagonized the salvarsan. Cardiac dilatation 
may also be directly produced by salvarsan and in such an event 
the heart shows changes in rate and volume before the blood- 
pressure falls. Sudden death following its administration is there- 
fore generallv a cardiac death (Luithlen). 3 The fatal termination 
has also been ascribed (Hoke and Rihl) to a central vasomotor 
depression. The administration of sodium arsenate produces a 
marked fall in blood-pressure without any direct effect upon the 
heart, showing that the action of salvarsan is not identical with 
that of arsenic. In vascular disease, doses which are not toxic to 
the heart may cause a sudden fatal termination through then- 
effect on the bloodvessels. Salvarsan causes contraction of the 
coronary arteries and a decreased pulse rate. 4 Rindfleisch has 
emphasized the danger of salvarsan injection in status thymo- 
lymphaticus, and has reported two cases in which a summation ot 
depression, salvarsan and thymus extract caused death. 5 

The depression of blood-pressure caused by salvarsan in medicinal 
dosage is never sufficiently great to endanger a normal circulatory 

. Intramuscular dose: cryst. strophanthin (ouabain) gr. T fc (0.0005 gram) , once 
i„ twenty-four hours. Intravenously in 1 to 6000 saline solution of strophanthin 
fBoehrineer) vs. , '„ to ,'„ (0.0005 to 0.001 gram). 

ESSSL MtaSLhdl and Stengel: The Influence of Temperature ■»"*£»- 
fcratloii on the Qualitative Reaction of the Heart to Ouabain, .lour. Phar. and Exp. 

1 U "IZ I.m !'r.' AnS der Salvarsanwirkung, Ztschr. 1. exp. Path. u. Therap., 1913, 

X "''< Iznbalski, I'.: AJbstr. « lentraJbl. f. d. ges. inn. Med., 1913, iv 149. 

. Rindfleisch, W.: Status Thymolymphaticusu. Salvarsan, Berl. khn. Wchnschr., 
1913, i. 542. 



Ill) ROW /■ A TRACT 355 

system, but this form of medication may be definitely dangerou 

in cases of marked hypotension. 1 

Neosalvarsan. During the administration of neosalvarsan both 
systolic and diastolic pressures, although variable, are usually 
increased apparently as a resull of excitement. After the injection 
(seven hours) both pressures arc decreased and remain so for 
several days. At first the systolic, later the diastolic, pri 
is most affected. 2 

Strychnin. Strychnin is still used in the treatmenl of symptoms 
associated with low Mood-pressure, especially it' the vasomotor 
depression is central iii origin. It acts reflexly and its beneficial 
effects arc indirect. It is capable of increasing the stimulability 
of the vasomotor system. 8 Like caffein, its effects are more pro- 
nounced if the blood-pressure is subnormal. Marvin 4 found a 
marked increase in pressure after doses of gr. .',, to ,',, i' 1 healthy 
students, but practically qo results from smaller doses. The pulse 
rate was invariably slowed, due recent investigations of New- 
burgh 6 have shown, however, that in infectious diseases in medicinal 
doses, strychnin does not increase the cardiac output, slow the 
pulse, or materially increase blood-pressure. Nor is strychnin 
of value as a heart stimulant in acute or chronic cardial- failure. 6 

Although the administration of strychnin may d<> g I. especially 

in essential hypotension, its effects arc due to its stimulation of the 
brain and spinal cord and not to any direct action upon the circula- 
tory mechanism. . 

Thyroid Extract. — Injected intravenously, thyroid extract pro- 
duces, as do the extracts of most tissues and organs, a fall of blood- 
pressure. It has been suggested that the hypotensive effect of 
thyroid substance is due to cholin, but Vincent believes that the 
depressor effect is due to other substances. 

Since a diminished thyroid secretion or an increased adrenal 
secretion tends to raise blood-pressure, and since these secretions 
appear to neutralize each other, and as exophthalmic goitre patients 
often have relaxed peripheral bloodvessels, the administration of 

1 Sieskind: Das Verhalten des Blutdruckes bei intravenosen Salvarsaninjek- 
tionen, Miinchen. med. Wchnschr., 1911, No. 11. 

2 Rolleston: Influence of Neosalvarsan on Blood-pressure, British Med. Jour., 
1915, ii, 285. 

3 Sollmann and Pilcher: Am. Jour. Physiol., 1912, xxx, 369. 

4 Arch. Int. Med., 1913, xi, 418. 

5 Newburgh, L. H.: Strychnin and Caffein as Cardiovascular Stimulants in Acute 
Infectious Disease, Arch. Int. Med., 1915, xv, 458. 

6 Newburgh, L. H. : On the Use of Strychnin in Broken Cardiac Compensation, 
Am. Jour. Med. Sc, 1915, cxlix, 696. 



356 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

thyroid gland seems justified as a therapeutic measure in hyper- 
tension. It stimulates thyroid secretion and cutaneous activity. 
It is best given in small doses, one to three grains daily. Such 
treatment is sometimes attended by beneficial results which not 
infrequently outlast its administration. The experiments of Reid 
Hunt indicate that some of the effects of diet are due to its action 
on the thyroid gland (see Exophthalmic Goitre, page 367). 1 

Vasotonin I Yohimbvn and Urethane). — The results reported upon 
the use of this drug are contradictory. Favorable action has been 
claimed both experimentally and clinically by some observers. A 
lowering of pressure without depression of the heart or vasomotor 
or respiratory centres has been reported. It is given in 1 c.c. doses 
daily or on alternate days, and may be administered hypodermically. 
It is said to cause less headache than the nitrites, 2 and to produce 
dilatation of the vessels in the extremities especially. It has been 
recommended for angina pectoris and arterial hypertension by 
Fellner 3 who reports favorable subjective and objective results. 
He states that it does not produce the aphrodisiac effects of yohim- 
bin, nor does it produce cardiac depression. 

Veratrum Viride. — Is employed by some physicians to lower 
blood-pressure in eclampsia. Just why, is difficult to understand, 
since the drug is not a vasodilator. In small doses it "exercises 
its effect upon blood-pressure neither peripherally through its 
action on the vessel walls, or on the vasomotor nerve endings, nor 
through a direct action on the vasomotor centre or on the heart, 
but reflexly through the afferent vagus fibers." 4 Clinically this 
drug has never been widely used because of its danger, uncertainty 
of action, and because its pharmacological status is still unsatis- 
factory. It is usually employed in the form of the tincture in doses 
of 10 to 20 minims. The effective therapeutic dose of the tincture 
of veratrum allium, according to Collins, 5 ranges between 30 and 
75 m. Such doses reduce the pulse rate from 12 to 42 beats per 
minute, and lower blood-pressure in both its phases about 30 mm. 
Ilg. In hypertensive cases the systolic pressure may be even more 
reduced, but the diastolic pressure is much less affected. 

1 Hunt: Jour. Am. Med. Assn., October 19, 1907, p. 1323; September 23, 1911, 
p. L032. 

- Muller and Fellner: Ueber Vasotonin, ein neuea druckherabsetzendes Gefaess- 
mittel, Therap. Monatshefte, 1910, xxiv, 285. 

■ Klinische Erfahrungen liber Vasotonin, Kong. f. inn. Med., 1910, xxvii, * » IT. 

•Cramer, W.: The Action of Veratrum Viride, Jour. Pharm. and Exper. Therap., 
1915, vii. 84. 

'■ Collins. H. .1. The Clinical Actions of Veratrum, Arch. Int. Med., 1915, xvi, 54. 



EFFECT OF DRUGS ON THE C0R0NAR1 IRTERIES 357 

Yohimbin. Pongs 1 reports in twenty-two cases after do i of 
0.r> to 2 cm. a slight fall of pressure followed by a secondary rise 
up to 35 per cent., reaching its high point in forty-five minutes 
and lasting one to five hours. No hypotensh e effects were demon- 
strable even with larger dosage; do untoward results uremia, angina 
pectoris were noted. Genital manifestation occurred <>nl\ twice. 

THE EFFECT OF DRUGS ON THE CORONARY ARTERIES. 

It seems evident, a priori, thai the local effed of different forms 
of medication upon the pressure and blood flow in the coronary 
arteries must be of extreme importance in the selection of our 
therapeutic remedies. The circulation in the coronary arteries 
is directly dependent upon blood-pressure. 

This question has been studied experimentally by noting (1) the 
contraction or relaxation of arterial strips, and (2) the amounl of 
blood flow from an opened artery. Such investigations have, 
however, not led to uniform results, because, as Rabe 2 pointed out, 
in either method the experimental heart is deprived of the effect 
of the central nervous system and is functionating under abnormal 
conditions. 

Voegtlin and Macht 3 found that digitoxin, digitalin, strophan- 
thin, and buffagin produced contraction, and that the nitrites and 
digitonin, digalen, dilatation of the coronary artery. If these 
findings hold good under normal conditions they would inameasure 
justify the coincident use of the nitrites with digitalis or strophan- 
thus. Rabe noted contraction from strophanthin, digitalin, epi- 
nephrin, and slight contraction from sodium nitrite and caffein. 
Myer's experiments (dogs and cats) corroborate the belief that 
epinephrin dilates the coronary arteries and increases blood flow 
through them. 4 Although this effect has been noted in numerous 
animals it appears that in the monkey and probably in man epi- 
nephrin causes coronary constriction. This is perhaps due to the fact 
that in the latter species the coronary arteries are supplied with 
constrictor nerves of true sympathetic (thoracicolumbar) origin. 5 
An increase of the C0 2 content of the blood causes dilatation of 

1 Ztschr. f. exp. Path. u. Therap., 1912, x, 479. 

2 Die Reaction der Kranzgefiisse auf Arzneimittel, Ztschr. f. exp. Path. u. Therap., 
1912, xi (bibliography) . 

3 Jour. Pharcn. and Exp. Therap., September, 1913. 

4 Myer: Zur Frage d. Adrenalin Wirkung auf d. Coronarkreislauf, Berl. klin. 
Wchnschr., 1913, 1, No. 20. 

5 Barbour, H. G., and Prince, A. L.: Influence of Epinephrin upon the Coronary 
Circulation of the Monkey, Jour. Exp. Med., 1915, xxi, 330. 



358 EFFECTS OF DRUGS ON BLOOD-PRESSURE 

the coronary arteries, together with cardiac dilatation and a fall 
of blood-pressure. Experimental asphyxia causes an even greater 
coronary dilatation, which increases in proportion to increased 
demands upon the heart muscle. 1 

INTRAVENOUS THERAPY. 

The increased employment of intravenous therapy warrants a 
brief mention of this topic here. While sometimes necessary and 
perhaps often advisable, the physician should not lose sight of the 
fact that aside from the possibility of introducing infectious material 
or of producing thrombosis, intravenous injections are often fol- 
lowed by a prompt and sometimes serious fall of blood pressure. 
This phenomenon which has been explained in the case of drugs 
as resulting from endocardial irritation, may occur after the intra- 
venous injection of substances which administered orally or intra- 
muscularly, have no such demonstrable effect. Quinine and 
potassium salts directly depress the heart muscle and sudden death 
has occurred following the use of iron preparations containing 
peptone. 2 

THE EFFECT OF MEDICATION ON VENOUS BLOOD- 
PRESSURE. 

The experiments of Capps and Mathews 3 carried out upon dogs 
under light ether anesthesia yielded the following results: 

The Digitalis Group. — The venous pressure was not materially 
altered. 

Epinephrin. — Small doses produced no effect. Large doses 
caused a rise of from 10 to 80 mm. The rise in venous pressure 
was coincident and coextensive with halting irregular heart action, 
and presumably the result of it rather than dependent upon veno- 
motor stimulation. 

Pituitrin. Acted similarly to, but more feebly than epinephrin. 

Caffein. This drug had no appreciable effect. 

Strychnin. Had no effect on venous pressure except in toxic 
in which it caused a rapid increase of pressure. 

The Nitrites. Both inhalation and injection of these substances 
causes a decided fall in venous pressure, due apparently to depres- 
sion nf the peripheral venous nerve endings. 

1 Markwalder and Starling: A Note on Some Factors which Determine the Blood- 
flow through the Coronary Circulation, Join*. Physiol., 1913, \l\ii, 27.",. 
Edit., Jour. \m. Med. Assn., November 11, 1916, p. 1450. 

J Vein, us Blood-pressure as Influenced by the Drugs Employed in Cardiovascular 
Therapy, Jour. \m. Med. Assn., 1913, lxi, 388. 



EFFECT OF DRUGS ON THE PI LMOh \U) YRTERl 359 

Morphin. This drug in small doses had little effect; in large 
doses it lowered venous pressure, bu1 not nearly to the extenl that 
did the nitrites. 

Alcohol. — Large doses increased venous pressure in proportion 
to the degree of cardiac and arterial depression produced. 



THE EFFECT OF DRUGS ON THE VASOMOTOR CENTRE. 1 

Aconite in non-toxic doses has no effect. Ergot and ergotoxin 
have practically no action. Ether may produce moderate stimu- 
lation but often is without effect. Strophantkus stimulates the 
centre moderately, whereas digitalis lias much less, if any, action. 
Neither of the last two drugs produce sufficienl effecl to influence 
the total action of the drug. Nicotin stimulates the centre. 
Spartein has no direct effect. Pituitary (infundibular) extract 
stimulates more frequently than it depresses, bu1 a direct effecl 
is generally not demonstrable. When effects do occur they are 
generally due to the rise in blood-pressure (stimulation of the vaso- 
motor centre) or to respiratory embarrassmenl depression of the 
centre). Hydrastin and berberin are apparently without action 
on the centre. Histamin has no direct action, bu1 a fall of pressure 
generally produces moderate stimulation. Chloroform produces a 
direct depression. The nitrites usually cause moderate stimulation, 
never a direct depression. The stimulation is probably due to the 
anemia caused by peripheral lowering of blood-pressure. Strychnin 
except in dangerously toxic doses exerts no effect, and even in such 
dosage stimulation may not be demonstrable. Camphor is likewise 
without effect. 

THE EFFECT OF DRUGS ON THE (ISOLATED) PULMONARY 
ARTERY. - 

Epinephrin causes powerful constriction. After ergotoxin and a 
number of other drugs the action of epinephrin is inhibited. These 
observations point strongly toward a vasomotor supply of the 
pulmonary artery. 

Digitalis. — With the exception of digitonin all of the digitalis 
bodies produce a constriction. Digitonin causes a dilatation. The 
nitrites cause a constriction of the pulmonary ring. 

1 Pitcher, J. D., and Sollmann, T.: Studies on the Vasomotor Centre, Jour. Phar. 
and Exp. Therap., 1914-15, vi. 

2 Macht, D. I.: Action of Drugs on the Isolated Pulmonary Artery, Jour. Phar. 
and Exp. Therap., 1914-15, vi, 13. 



CHAPTER XV. 

METABOLIC DISEASES AND MISCELLANEOUS 

CONDITIONS. 

Diabetes. — Experimental Evidence. — Recent researches indicate 
that glycosuria is in some way related to the secretion of the adrenal 
glands. Sugar excretion can be induced by the injection of epi- 
nephrin. The latter also produces a marked rise of blood-pressure 
through vasoconstriction. Neubauer's 1 investigations have shown 
that other substances which raise blood-pressure (e. g., barium 
chloride) may also induce glycosuria, whereas narcotic drugs, 
opium, chloral, alcohol, etc., which tend to lower blood-pressure, 
may diminish or prevent the occurrence of glycosuria after puncture 
of the roof of the fourth ventricle. It has further been shown that 
when sugar excretion is brought about by vasoconstrictor drugs 
it is associated with marked hepatic hyperemia. A local stasis 
of blood in the liver will, it seems, bring about this liberation of 
glycogen in the form of glucose, with an attendant hyperglycemia 
and a glycosuria. It appears that transient glycosuria may be 
brought about by the same emotional states — pain, rage, fear, 
excitement — as those which cause an increased outpouring of epi- 
nephrin into the blood stream. Until the pathogenesis of diabetes 
has been more thoroughly established no definite conclusions 
regarding the relationship of arterial hypertension to this disease 
can be drawn. The evidence at hand, however, suggests that a 
general vasoconstriction, when accompanied by a local vasodila- 
tation of the hepatic vessels, may account for some cases of glyco- 
suria. Ilagelberg found the sugar content of the blood abnormally 
high in twenty-six cases of nephritis or arteriosclerosis, and suggested 
that an increased adrenalin content of the blood accounts for both 
the hyperglycemia and the hypertension. 2 It is more likely, how- 
ever, that the relationship between hypertension and glycosuria 
is not ;i causal one. There is no constant relation between blood 

1 Uebor (1. Wirkuiif!; antiglycosurisclier Mittcl u. iiber Leberglucosurie, Biocbem. 
Ztschr., L912, xliii, 335. 

Bagelberg: BerL klin. Wchnschr., October 7, 1912. 



DIABETES 361 

sugar ami blood-pressure, nor is there a sufficient reason for assuming 
that these two conditions are dependent upon a common et iological 
factor (epinephrin). (See Hyperglycemia, page 295.) 

Clinical Consideration. Diabetes hears no constant relation to 
blood-pressure,. ( lases occurring in advanced life often show hyper- 
tension as the result of renal and cardiovascular arteriosclerosis, 
which is commonly associated. This is illustrated by the following 
tables published by Joslin: 1 

The A\i.i;\*.i: I'.i.oun i'ici>si i.i> m N'humai. and Diabetic Individuals. 



Norm 


al Individuals 


\\ i i 


Diabetic Patients 


Average 




(Fisher) 




blood- 








blood- 


. Ages. 




Number. 


pressure. 


Ages. 




Number. 


pressure 


15 to 20 




. 2S1 


120 


15 to 20 




38 


121 


21 to 25 




. 7 s.-, 


123 


21 to 25 




33 


122 


26 to 30 




. 791 


124 


26 to 30 




56 


121 


31 to 35 




689 


124 


31 to 35 




39 


120 


36 i" in 




. 2,111 


L27 


36 to 40 




r,l 


li'.-, 


41 to 45 




6,740 


L29 


11 to 15 




75 


139 


46 to 50 




. 1,171 


131 


46 t" 50 




116 


l 13 


51 to 55 




. 2,371 


L32 


51 to 55 




127 


154 


56 to 60 




. 1,100 


135 


56 to 60 




L03 


154 










Over c,ii 




. L63 


15G 



19,339 127 Ml 139 

Joslin encountered a fall of pressure coincidently with a disap- 
pearance of glycosuria only once in Ml cases. He suggests that 
the high blood-pressure in diabetics past forty years of age i- d in- 
to arteriosclerosis possibly induced by the high protein feeding 
formerly in vogue. 

I once had under my care a gentleman of sixty-eight years, 
with a blood-pressure of 185-85 mm., who had long been diabetic. 
Having made a careful study of his own case he had succeeded in 
keeping himself sugar-free by careful dieting and severe muscular 
exercise. He had made the observation that if he performed enough 
physical work to induce copious perspiration he could metabolize 
a certain amount of glucose, which otherwise was excreted by the 
kidneys. 

All went well for several years until he developed angina pectoris 
which prevented his exercise. He said to me one day, " If I exercise 
I shall die of angina pectoris, if I do not exercise I at once develop 
acidosis. I have the chance, not offered to many men of choosing 
between two varieties of dying." He chose angina and died two 
months later. 

!The Treatment of Diabetes Mellitus, Philadelphia, 2d ed., 1917, p. 413. 



:"!• »2 ME T. 1 BOLIC DISEASES AND MISCELLANEOUS CONDITIONS 





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GOUT 363 

Diabetes in the young is accompanied by normal pre iir< 
In the later stages hypotension may occur. Blood-pre ure e tima- 
tions may be of diagnostic value in differentiating between diabetic 
and uremic qoma. In the latter condition hypertension is the rule 
until the terminal fall of pressure occurs, whereas diabetic coma is 
associated with hypotension. 1 Although this occurs less constantly 
than does hypertension in uremia, it is sometimes an early mani- 
festation. The so-called " diabetic collapse" which has been believed 
to occur independently of eoiua, appears to be the result of a rapid 
fall in blood-pressure due to cardiac and vasomotor weakness, 
resulting from acidosis. Experimentally the injection of /3-oxy- 
butyric acid causes a fall of blood-pressure. 

The pulse rate is increased in diabetes, and. as has been empha- 
sized by Benedict and Joslin, stands in intimate relation with 

increased metabolism. 2 Preceding the onset of coma, bl l-pressure 

falls sometimes ID to 50 nun. Hg. Decrease of intra-ocular tension, 
which occurs simultaneously, is well known and results, in part 
at least, from the lowered arterial tension. Blood-pressure readings 
are therefore of value in detecting the onset of coma as well as in 
indicating treatment. It has been found that in coma cases with low 
blood-pressure better results are obtained when cardiovascular 
stimulants are combined with the usual alkaline therapy. The 
administration of thyroid substance to diabetics often causes a 
rise of blood-pressure (Biedl). 

Gout. — Until the pathogenesis of gout is more definitely eluci- 
dated it is impossible to make positive statements in regard to 
the relation of this disease to arterial hypertension. It seems that 
the products of protein metabolism, if increased or abnormal in 
character owing to overeating, suboxidation, or faulty excretion, 
may produce hypertension. Occasionally metabolic intoxication 
seems to lead to hypotension. High pressure is, of course, the rule, 
with added increments of tension during the acute attacks (pain), 
but -gout is very commonly associated with arteriosclerosis and 
chronic nephritis. The latter certainly accounts for a measure, 
if not all, of the increased blood-pressure. Hypotension is some- 
times seen in the later stages in association with cachexia, acidosis, 
and cardiac weakness. It has also been described as occurring 
at the onset of an acute attack. The presence of hypertension 
may be of some value in diagnosticating between lesions of the 

1 Ehrmann, R. : Ueber cardiovasculare Symptome u. d. Therap. bei diabetischem 
Coma u. Praecoma. Berlin klin. Wchnschc, 1913, 1, 11, 1423. 

2 Metabolism in Severe Diabetes, Carnegie Institute of Washington, 1912, Pub. 
176, p. 85. 



364 METABOLIC DISEASES AXD M I S< ELLAS EJUS ( OX 1)1 TIONS 

joints, skin, eye, etc., as to whether they be tuberculous or gouty 
in origin. 

Experimental Data.— Investigations point strongly to the conclu- 
sion that the occurrence of gouty symptoms is closely associated 
with abnormalities of protein metabolism, expecially with that 
portion of it which relates to the breaking down and elimination 
of the aniino-acids. 

In animals the intravenous injection of guanin (0.02 to 0.03 gm. 
per kilo) causes a fall of blood-pressure of from 2.4 to 4 c.c. Hg. If 
other substances are employed which stand chemically near to 
guanin but have no amino group, c . g., xanthin, uric acid, an increase 
of pressure results (0.7 to 2.6 cm. Hg.). In the transition from 
guanin to uric acid there is a splitting off of the animo group, to 
which guanin probably owes its pressor effect. 1 

Jaundice. — Jaundice is often associated with hypotension. 
According to Federn, the latter can often be demonstrated before 
the bile appears in the urine. 

Experimentally a small amount of bile in the blood depresses 
cardiac contractility and slows the rate. Large quantities increase 
contractility but shorten diastolic relaxation. Paradoxically it 
would seem, these changes are more pronounced when the heart is 
fatigued or diseased. - 

Addison's Disease. — Arterial hypotension is frequently but not 
invariably found in Addison's disease. It bears no relation to the 
degree of pigmentation, but is believed to occur when the medullary 
portion of the adrenal gland is diseased. This tends to corroborate 
the belief generally held at present that the adrenal secretion may 
raise blood-pressure, but that it is not under normal conditions 
the sole cause of its maintenance, 3 and further, that Addison's 
disease results not merely from degeneration of the adrenal glands 
but from involvement of the entire chromaffin system. 

Grunbaum found the oral administration of epinephrin, while 
it did not raise blood-pressure in health, did so in case of adrenal 
insufficiency. He suggests the use of this substance as a diagnostic 
test. Together with careful blood-pressure readings, three grains 
of adrenalin are administered thrice daily. Any distinct subsequent 



1 Degree and Dorleans: Influence do la constitution des corps purques sur leur 
action vis-a-vis dc la prcssion artcrielle, Compt. rend. Acad, des Sciences, Paris, 
L913, elvi, 93. 

'• I'.crti. A.: Colemia Sperimentale, Gaz. d. Osped. e. d. Cliniche, 1916, xxxvii, 1236. 

1 Huskiiis. R, <',.. and Rowley, W. X.: The Effects of Epinephrin Infusion on 
Vasomotor Irritability, Am. Jour. Physiol., 1915, xxxvii, 471. Cannon, W. B.: 
Bodily Changes in Pain, Hunger, Fear, Rage, New York, 1913. 



AUTO i\ r<>\ i< \ i n>\ 365 

rise of pressure in the absence of a valvular lesion is, he believes 
suggestive of Addison's disease even in the absence of asthenia and 
pigmentation. Too much reliance must not be placed upon this 
test. 

On the other hand, recent experiments have shown that a fall 
of pressure occurs after the injection of dilute solul ions of epinephrin, 

and that hypertension occurs onlj when ab mally large doses 

are used. In amounts sufficient to raise blood-pressure, intestinal 
peristalsis is completely inhibited. If these observations are cor- 
rect the low pressure seen in adrenal insufficiency and in Addison's 
disease are probably due rather to an interference with muscular 
metabolism, including that of the heart and the arteries, than to 
failure of a normal tonic stimulation of the sympathetic nervous 
system. 1 

Auto-intoxication. Much has l>ccu written and but little is 
known regarding gastro-intestinal auto-intoxication. The literature 
on the subject is enormous and concerns itself mainly in nebulous 
hypothecation. It has been shown that two pressor bases may 
be extracted from putrid meat, and the assumption that they 
are generated in the intestine through bacterial action seems 
probable. Granger was unable to confirm tin- observation of 
Abelous and Bain that the normal urine contains pressor bases, 
and there is as yet no definite clinical proof that these urinary 
pressor substances are identical with those isolated from decaying 
proteids. 2 

Hydroxyphenylethylamin is a substance which can be prepared 
from tyrosin, a derivative of protein cleavage, by splitting oil' 
carbon dioxide from the tyrosin molecule. This reaction may be 
caused by putrefactive bacteria. Hydroxyphenylethylamin has 
been isolated by Barger 3 from putrefying proteids and shown 
to have a pressor action. The group of aromatic am ins to which 
it belongs is related chemically to epinephrin. It is an interesting 
fact that this aromatic amin (p-hydroxyethylamin) with its blood- 
pressure-raising qualities is found in epinephrin, in ergot, and as 
the result of bacterial putrefaction. "Our poisons and our drugs 
are in many instances the close relatives of harmful compounds that 

1 Hoskins and McClure: Am. Jour. Phys., 1912, xxi, 59. Hoskins and McPeck: 
The Effect of Adrenal Massage in Blood-pressure, Jour. Am. Med. Assn., 1913, 
lx, 1777. 

2 Granger, A. S.: Concerning the Presence in the Urine of Certain Pressor Bases, 
Arch. Int. Med., 1912, x, 202. 

3 The Isolation of Pressor Principles of Putrid Meat, Jour. Physiol., 1908, xxxviii, 
341. 



366 METABOLIC DISEASES AND MISCELLANEOUS CONDITIONS 

represent the intermediary steps in the daily routine of metabolism." 

As Abel 1 has recently stated, "It would appear that we have at 
last got onto the right road for the chemical investigation of alimen- 
tary toxemia and its alleged consequences, such as arteriosclerosis 
and chronic renal disease. Phenylalanine, tyrosin, tryptophane and 
histidine, the harmless precursors of toxic amins are always present 
in the intestine, and when they are acted upon by an excessive 
number of certain microorganisms the resulting toxic bases will 
surely be formed in excess. It' they are then taken up into the blood 
in quantities too large for transformation by the liver or other 
defensive organs, into harmless derivations, they must inevitably 
manifest their pharmacological and toxicological properties." 

Not only arterial hypertension but also hypotension has been 
clinically attributed to alimentary toxemia. That the latter no 
less than the former may have basis in fact is shown by the 
observation of Barger and Dale- who were able to obtain a highly 
toxic depressor base — B-amino-azolylethylamin from the intestinal 
mucosa. 

This substance appears to be formed from histidine through the 
agency of the B-aminophilus intestinalis. 3 It has further been 
suggested that the toxic substance which causes anaphylactic 
-hock bears an allied chemical composition. 

The Effects of Glandular and Tissue Extracts. — The extracts 
of most animal tissues when injected intravenously lower blood- 
pressure. It has been suggested that in many instances this 
depressor action is due to cholin, a substance abundantly found in 
brain-tissue extracts and in tissues in which proteolytic changes, 
which occur very early, have taken place. The action of cholin 
is characterized by the fact that the first injection fails to establish 
tolerance to a second injection, and by the fact that the reaction 
may he counteracted by atropin. The depressor effects of peptone 
have long been known, but in this case tolerance is established 
by the first dose 1 (see Toxic Shock, page 219). 

Certain glandular extracts have also been shown to possess a 
specific action on blood-pressure. Thus extract of the adrenals 
and hypophysis possess well-marked pressor effects, while pineal 
and thyroid extracts cause a fall of pressure. 

1 The Blood and the Specific Secretory Products of the Organs of Internal Secre- 
fcion, Science, L915, N. S., xlii, 165. 

2 Jour. I'!, vmm]., HUM, xl, 38. 

Bertheloi and Bertrand: Compt. rend, de L'Acad. d. Sciences, 1826, cliv, 1643. 
'Sanford and Blackford: Comparative Study i>f the Effects on Blood-pressure 
of the Extracts and Serums of Exophthalmic < Jcitre and other Substances, Jour. Am. 
Med. ,\ ,,.. 191 i. Imi. i ir (bibliography). 



EXOPHTHALMIC GOITRE 367 

Acromegaly. In acromegaly pressure is variable (see Pituitary 
Extract, page 352). Chromic hypopituitarism, both clinical and 
experimental, is characterized by a deposition of fat, a lowering of 
body temperature, a retardation of the pulse and respiratory 
rates, somnolence and lowered blood-pressure. These symptoms, 
as has been pointed out by Cushing and Goetch, 1 bear a striking 
resemblance to the state of hibernation as it occurs in some animals. 
W. Landon Brown' 2 states thai in the earlj tages of acromegaly 
in association with hemianopia, lowered sugar tolerance and osseous 
hypertrophy, blood-pressure is high, whereas in the later stages 
with a high sugar tolerance blood-pressure is low. In Frolich's 
syndrome (primary hypopituitarism) smooth, dry skin, scant pubic 
and axillary hair, small, thin finger-nails blood-pressure is low. 

Exophthalmic Goitre. Experimental Data. In 1894 Oliver and 
Schafer reported that the intravenous injection of aqueous or 
glycerinized extracts of the thyroid gland produced a fall of blood- 
pressure in which the heart took no part. These observations 
have been widely corroborated. A few observers found an increased 
pressure and local vascular constriction after thyroid injections. 
The pulse rate has been reported both as accelerated and retarded. 

Von ('yon and Oswald found lowering of pressure and slowing 
of the pulse after the intravenous injection of iodothyroid even 
after atropinization and section of the vagi. Later experiments 
have shown that the effect of this substance upon cardiac inhibition 
is questionable, and that the fall of pressure is not a specific action, 
but occurs after the injection of many organic extracts which 
contain cholin, a substance which is associated with the metabolism 
of lecithin and other lipoids, and to which the fall of blood-pressure 
is due. On the other hand, it has been maintained that the fall of 
pressure is not due to a cholin but to a specific substance, vaso- 
dilatonin (Popielski), which acts even after atropinization. This 
substance seems not to be a specific thyroid product. In contra- 
distinction to the equivocal results in dogs and rabbits, in cats 
iodothyroid produces a marked lowering of blood-pressure which 
is due to both vascular and cardiac action; but here again it seems 
that similar effects may be produced by other iodized albumins. 
Therefore the contention of von Cyon that iodothyroid possesses 
a fundamental cardiovascular regulatory function has not been 
substantiated, nor has the hypothesis that the cerebral circulation 
is controlled by an interaction between the thyroid, hypophysis, 

1 Jour. Exp. Med., 1915, xxii, No. 1. 

2 Physiological Principles in Treatmen t, 'London, 1914 ,'p. 34. 



368 METABOLIC DISEASES AND MISCELLANEOUS CONDITIONS 

and pineal glands any better foundation. The intravenous injection 
of thyroid extract in cats and rabbits increases the stimulability 
of the depressor function and the rise of pressure produced by 
adrenalin (Hiedli. 1 More recently Kendal has isolated a crystalline 
compound ulpha iodin — which appears to be the active constit- 
uent of thyroidal secretion. He has made some interesting obser- 
vations regarding its effect on the circulation. For several hours 
after its administration no effect upon blood-pressure or pulse rate 
is noted, but if amino-acids are simultaneously injected the pulse 
rate is enormously increased. It would seem that the increased 
pulse rate is a response to the demands of greatly stimulated 
metabolism. - 

The oral administration of thyroid substance in man produces 
an increased pulse rate and often a fall of blood-pressure; in 
diabetics a rise of pressure occurs which outlasts the employment 
of the medication by several days. The prolonged use of thyroid 
usually produces similar effects, although both experimentally and 
therapeutically the results are inconstant and have again been 
explained as not due to specific thyroidal action (Biedl). Blackford 
and San ford found that a powerful depressor substance exists in 
exophthalmic goitre cases and that a primary injection establishes 
tolerance to the action of any further administration. Atropin 
does not inhibit its action, but heating to 70° C. does, hence the 
substance does not behave physiologically like cholin. The action 
is chiefly the result of peripheral vasodilatation associated with 
some diminution of the systolic output. Irritability of the vagus 
is not decreased. The existence of a crossed tolerance between 
the depressor action of extract of exophthalmic goitre and of serum 
from patients suffering from this disease suggests that the two 
substances are identical. 3 

Clinical Data. — The earlier reports of blood-pressure findings in 
exophthalmic goitre are very variable, some observers having noted 
hypertension, while others found hypotension or normal pressures. 
This is largely due to the fact that only the systolic pressure was 
estimated. More recenl investigations by Plummer and by Taussig 
have shown that in toxic goitre the systolic pressure is usually 
increased while the diastolic pressure remains normal. Thus the 
pulse-pressure is large. 

1 Innere Bekretion, 1913, i, 205. 

2 Kendall, E. C: Recenl Advances in < >ui Knowledge of the Active Constituent in 
the Thyroid. lit- Clinical Nature ami Function, Boston Med. and Surg. Jour., 
< >< tobex 19, L916, Hxxv. 

3 Blackford, .1. M., and Banford, M. D.: Med. Record, 1913, lxxiv, 379. 



EXOPHTH ILMIC GOITRE 



369 



The clinical picture of toxic goitre has much iii common with 
that of aortic insufficiency. Increased pulse rate, pulsus cehr, 
capillary pulse, throbbing arteries, cardiac hypertrophy, arterial 
sounds and the persistence of the fifth auscultatory pha 
common to both conditions. In addition Taussig 1 has shown that 
differences in the arm and leg pressures affecting the systolic and 
the pulse-pressure occur quite uniformly in toxic goitre. The pop- 
liteal pressure in recumbency is higher than thai in the brachial 
arteries. This is in marked contrast to the findings in non-toxic 
goitres in which the pressures in the upper and lower extremities 
are strikingly identical. The incessant pounding to which the 
arteries in toxic goitre are subjected leads to sclerotic changes, and 
Plummer believes that these cases in time develop chronic arterial 
hypertension. 



Average Blood pressure hy Half decades; Mon hyperplastic Goitre. 
(Plummer.) 



years. 
10 to 15 
15 to 20 
20 to 25 
25 to 30 
30 to 35 
35 to 40 
40 to 45 
45 to 50 
50 to 55 
55 to 60 
60 to 65 
65 to 70 
70 to 75 
75 to SO 



Number of 
cases. 

15 

63 
128 

190 
l'.;:, 
253 
246 
21 1 
204 
131 

47 

13 
4 



systolic 
blood-pressure. 
lis..", 
120.7 
L23. l 
123. 8 
L26 9 
134.9 
L36 I 
l 15 8 
150.2 
152.6 
160.7 
164.6 
166.2 
106.0 



Average diastolic 
blood-pressure. 
72.r» 
77.7 
80.2 
80.5 
81.2 
83.6 
85.2 
87.3 
87.1 
87.5 
88.6 
83.3 
87.5 
65.0 



Average Blood-pressure by Half-decades; Hyperplastic Goitre. 
(Plummer.) 

Number of Average systolic Average diastolic 

Years. cases. blood-pressure. blood-pressure. 

10 to 15 14 138.5 68.8 

15 to 20 5S 139.4 75.9 

20 to 25 110 137.8 70.7 

25 to 30 164 139 . 6 75 . 2 

30 to 35 139 140.8 78.7 

35 to 40 106 155.2 75.6 

40 to 45 93 145.1 76.7 

45 to 50 94 153.1 77.8 

50 to 55 ..'... . 47 152.4 77.0 

55 to 60 17 160.6 77.7 

60 to 65 5 160.0 71.2 



1 Some Blood-pressure Phenomena in Exophthalmic Goitre, Tr. Assn. Am. Phys 
1916, xxxi, 121. 
24 



370 METABOLK ! DISEASES AXD MISCELLANEOUS CONDITIONS 

Percentage of Cases oveh Forty Years of Age Having High Blood- 
pressure. (Plummer.) 

Systolic blood- Systolic blood- 
Nun. her of pressure above pressure above 
150. 160. 

Hyperplastic jioitre .... 117 47 34 

Non-hyperplastic goitre . 417 35 27 

Cholecystitis with stones . . 289 .. 18 

Uterine myoma 100 25 15 

Positive Wassermann . 100 21 14 



Showing Percentage of Cases by Decades, Having a Blood-pressure 
Above 160. (Plummer.) 

Age, Age, Age, Age, Age, Age, 

10 to 20 20 to 30 30 to 40 40 to 50 50 to HO 60 to 70 

years, years. years. years, years, years. 

percent, percent, percent, percent, percent, percent. 

Hyperplastic goitre . 12 17 22 30 37 30 

Non-hyperplastic goitre 1 2 7 21 31 20 

The preceding tables taken from Plummer 's 1 publication show the 
systolic and diastolic readings obtained from a large series of goitre 
cases. It is evident from the diastolic pressures that there was 
no vascular hypertension in these cases. 

Plummer construes the high systolic pressure as an effort to main- 
tain a normal diastolic pressure despite widely dilated arterioles, 
by an increased systolic output and an accelerated rate. In other 
words, the pulse-pressure is large and the diastolic pressure remains 
normal because even the widely opened arterioles cannot with 
sufficient rapidity carry off the tremendous cardiac output. He 
further believes that in exophthalmic goitre the height of the sys- 
tolic pressure is an expression of the degree of intoxication. This 
intoxication which causes the high systolic pressure although often 
transitory, later leads to diastolic hypertension and in time to 
permanent cardiovascular changes. 

As might be expected from the symptoms of this disease, flushing, 
warmth, perspiration, and a rapid pulse, blood flow is rapid. Stewart 
found in a case studied by him that immersion of one hand in cold 
water reduced the flow in its fellow from 14 to 7 gm. per 100 cc. 
per minute. Weber found that in exophthalmic goitre and in neuras- 
thenia there was a tendency for the normal vasomotor reflexes 
associated with attention and the suggestion of movement to be 
readily lessened or even reversed. In other words, fatigue phe- 
nomena occurred more readily than in normal eases. 

McCrea lias called attention to a special type of exophthalmic 
goitre associated with a gain in weight, an increased blood-pressure 



I'.i i 



-pressure and Thyrotoxicosis, Tr. Assn. Am. Phys., 1915, \xx, 450. 



STATUS I.) WPHATICUS 371 

(200)j a high lymphocytosis and drowsiness, [mprovement occurs 
under the use of thj mus ex1 rad . 

Kaess 1 found the viscosity of the blood in exophthalmic goitre 

normal in li' per cent., decreased in 50 per cent., and increased in 
31 per cent, of his cases. The latter occurred in t he vagotonic cases 
and probably resulted from increased perspiration, diarrhea, etc. 
Diminished viscosity occurred in the sympathicotonic cases and 
was perhaps due to abnormality of the serum. Hemic viscosity, 
however, hears no constant relation to blood-pressure. 

Myasthenia Gravis. In a case reported by Bookman and 
Epstein, and associated with cutaneous bronzing, the sj stolic blood- 
pressure ranged between 215 and L90; the diastolic pressure between 
170 and 1 10 mm. 2 

Periarteritis Nodosa. Although Meyer, in 1878, believed that 
this disease was due to high blood-pressure which caused a rupture 
of the arterial media, recent investigations poinl to an infectious 
origin. In 5 of the 38 cases of this disease collected l>y Lamb 3 the 
blood-pressure readings were reported as l LO, 215, 77 LOO, L30 165, 
KM, therefore showing no constant relationship. 

Myxedema. In myxedema blood-pressure is generally increased. 

Adiposity.- Adiposity is not associated with any constant blood- 
pressure abnormalities. When the circulatory system is normal 
a loss of weight entails no fall of pressure, but if hypertension i> 
associated with adiposity a reduction of weight produces a fall of 
pressure, 4 largely, it would seem, owing to a diminution of metabolic 
waste products which result from overeating. (See p. 278.) 

Scurvy. —The Capillary Resistance Test. — In the earl\ stages of 
scorbutus, even before other clinical manifestations have occurred, 
a cuff applied to the arm and kept inflated for three minutes will 
cause the appearance of petechial spots. 5 The test is of course 
not specific for scurvy but merely indicates the resistance of the 
capillaries to pressure. 

Status Lymphaticus. — In status lymphaticus we have to do with 
an individual who is constitutionally subnormal. The muscular 
physique is poor and the physical strength and constitutional 
resistance below the normal standard. The blood-pressure is apt 
to be somewhat lower than the subject's age and weight would 

1 Brims: Beitr. z. klin. Chir., 1912, lxxxii, 253. 

2 Bookman and Epstein: Metabolism in a Case of Myasthenia Gravis, Am. Jour. 
Med. Se., 1916, cli, 267. 

3 Periarteritis Nodosa, Arch. Int. Med., 1914, xiv, 481. 

4 Dunin, Th.: Der Blutdruck in Verlaufe d. Arteriosclerose, Ztschr. f. klin. Med., 
1904, vol. liv. 

5 Hess and Fish: Infantile Scurvy, Am. Jour. Child. Dis., 1914, viii, No. 3. 



: 172 ME TABOLIC DISEASES AND MISCELLANEOUS CONDITIONS 

lead us to expect. According to Muenzer hypotension is found 
associated with lymphocytosis. While this may hold good for 
extreme cases, certainly lymphocytosis has not been shown to be 
a constant phenomenon in adults, not, so far as we are aware, in 
children. Operative procedures in this class of cases are dangerous, 
especially if chloroform is used as an anesthetic. The toxemia of 
acute infectious disease is also badly borne by these patients. 
Sudden and unexpected death during anesthesia, infections, while 
swimming, or in children while quietly resting in bed, appears to 
bear a relation to enlargement of the thymus gland. The experi- 
mental intravenous injection of thymus substance lowers blood- 
pressure, but whether this results from vasomotor depression or 
from purely mechanical causes (embolism, thrombosis), as suggested 
by Popper, 1 is uncertain. It may also be simply the non-specific 
fall of pressure which attends the intravenous introduction of 
different foreign proteids. 

Anemia.— Experimental Data.— Loss of blood tends to cause a 
fall of blood-pressure. When hemorrhage has been moderate this 
tendency is compensated by reflex vasomotor constriction and an 
increased pulse rate; when excessive, death occurs with a progres- 
sive fall of pressure, owing to cerebral anemia. 

The quality of the blood exerts an influence on vascular tonus 
and blood-pressure. Lesser found that section of the cord between 
the second and fourth cervical vertebras caused a fall of pressure 
and a diminution of hemoglobin in the large vessels, whereas 
stimulation of the sectioned cord increased the hemoglobin. Section 
above the splanchnic centre diminishes the erythrocytes (Cohnheim 
and Zuntz). Experimental epinephrin hypertension (in dogs) 
increases the red cells in the capillaries and veins but not in the 
large arteries. According to Erb the arterial and venous hemic 
concentration increases with a rise and decreases with a fall of 
pressure. Holobuts attributes the variations of the number of 
erythrocytes to changes in the volume of the corpuscles. The 
dried residue and the plasma show but little change with pressure 
variations (Horner). 2 

Clinical Data. Blood-pressure observations in the different forms 
of anemia are of little value, except in the detection of nephritic 
complications. If the anemia is marked, pressure will be low in 
proportion to the cachexia and general weakness. Chlorosis is 

i Ueber d. Wirkung d. Thymus extrakts, Sitzungsber. d. k. Akad. d. Wissensch., 
1905, rariv. 

»Der Blutdruck d. Menschen, Vienna, 1913, p. 101. 



EFFECTS OF HIGH ALTITUDES ON BLOOD-PRESSURE 373 

said to be accompanied by slight hypertension in the early stages, 
followed later, if its course be prolonged or severe, by hypotension. 
Blood-pressure bears no constant relation to either the percentage 
of hemoglobin or to the total number of corpuscles. According to 
Plesch the minute volume of the neari is increased in the anemias. 
Stewart found peripheral blood How in anemia less than normal. 
This peripheral constriction has been construed as a necessary 
compensatory arrangement for increasing blood flow through the 

lungs. The deficiency in the hand How is less in chlorotic anemia 
than in the other forms. Mnenzer' found lymphocytosis frequently 
associated with arterial hypotension. In pernicious anemia very 
low readings are often observed. Cabot states thai systolic pressures 
of SO and even 60 mm. are not unusual. 

Cachexia.— Nutritional failure from whatever cause is often 
associated with low arterial pressure, hut this is by no means 
invariably the case. The high pressures of nephritis may he some- 
what reduced by the coincident presence of cachexia. A remarkable 
case of persistent hypotension has been reported by Rolleston: 2 
that of a man with carcinoma of the tongue and amyloid disease 
who managed to live for several weeks with systolic and diastolic 
pressures of 70 and 35 respectively. 

The Effects of High Altitudes on Blood-pressure. The disturb- 
ances of physiological function which result from high altitudes are 
mainly due to a deficiency of oxygen. The vertigo, confusion of 
the senses, and fatigue can he abated by the inhalation of oxygen. 
At altitudes of from 4000 to 8000 meters (13,000-26,000 feet) 
no special precautions are necessary, provided the partial pressure 
of the oxygen in the lungs is raised. Beyond this special devices 
insuring adequate oxygenation must be employed. Mountain 
sickness results from a combination of diminished oxygen supply 
associated with muscular exertion, producing syncope, a weak 
pulse, and other symptoms of cerebral anemia. Circulatory symp- 
toms are especially apt to occur in aviators if very rapid ascents or 
descents are made. 

Henderson's studies made on Pike's Peak (14,000 feet) showed 
that there was a slight fall of arterial pressure. It seems to be 
generally agreed that altitude of a considerable degree does tend 
to lower blood-pressure and to increase the pulse rate, and that 
these changes are more marked at first, i. e., before "acclimatiza- 

1 Blutdruck u. Blutbild, Med. KHnik, 1913, ix, 2028, 2074. 

2 Low Blood-pressure in Carcinoma of the Tongue with Amyloid Disease, Lancet, 
September 12, 1914, p. 692. 



374 METABOLIC DISEASES AND MISCELLAXEOUS CONDITIONS 

tion" has taken place. Such a fall of pressure may range between 
1 and 22 nun., and the effects are naturally more marked in hypo- 
tensive individuals. There is, however, a great difference in indi- 
vidual susceptibility. The systolic pressure is chiefly and more 
constantly affected, and diastolic pressure may even rise. Ordinarily 
slight elevations produce but little change in blood-pressure. It 
is quite impossible either from a. man's general physique or from 
any other criterion to forecast how much his pressure may be 
affected. 1 The rate of blood flow was increased from 30 to TOper 
cent., by residence at Pike's Peak ( 14,000 feet). This was associated 
in part with an increased pulse rate and a fall of venous pressure. 
The arterial pressure was not clearly altered either by altitude or 
by oxygen inhalations. The latter did slow the pulse rate 14 per 
cent, at 14,109 feet, and .">! per cent., at 0000 feet. 2 All three of 
these factors are more increased by exercise than at lower levels. 
Furthermore, the stimulating effect of the low barometric pressure 
is more marked, the more vigorous the exercise, because although 
pulse and arterial pressure increase the venous pressure rarely 
exceeds the normal for low altitudes. A short sprint increased the 
systolic pressure on an average 01 mm. (Schneider). The pulse 
rate remains high for a longer time after cessation from work and 
the period of postexercise subnormal systolic pressure is increased. 
In brief, exercise at high altitudes is much more taxing upon the 
circulatory apparatus than at lower levels, and hence the danger 
of permanent as well as immediate damage is especially to be 
considered by (1) the unacclimated; (2) the non-robust, and (3) 
individuals who have cardiovascular lesions. 3 The readings obtained 
by ("lough at an elevation of over 5000 feet were practically iden- 
i ical with those taken at the sea level. Miners in suddenly descend- 
ing or ascending 1700 feet to and from their work show variations 
hardly exceeding 5 mm. Hg. 4 Hess 5 has attempted to explain 
the changes in blood-pressure at high altitudes by the fact that 
the normal balance between the concentration of the arterial and 
the venous blood (which he believes is normally regulated by the 
lungs) is upset. 

'Schneider and Hedblom: Blood-pressure, with Special Reference to High Alti- 
tudes, Am. Jour, Physiol., L908, mriii, '.»(). 

'Schneider, E. E., andSisco, D.I..: Circulation of the Blood a1 High Altitudes, 
Am. Jour, Physiol., 1914, xxxiv, 1 (literature), 

3 Schneider, < heley and Sisc<>: Am. .lour. Physiol., 1916, xl, No. 3. 

1 Clough, 1'". E.i Blood-pressure Variations as Influenced by Rapid Changes in 
Altitude. \p-L. lin Med., 1913, \i, 590. 

■Die Beeinflussung d. Plussigkeits anstauches zw. Blut. u. Geweben durch 
Schwankungen d. Blutdrucks, Deutsch. Arch. f. Win. Med., l'.)()4, lxxix, 128. 



EFFECTS OF TROPICAL CLIM \ri: 375 

Doubtless many of the contradictor} statements regarding the 
effects of altitude on blood-pressure arc due to1 be fact I hal normal 
and abnormal subjects have been classed together. 'Tims among 
tuberculous patients an elevation of 6000 feel appears to increase 
blood-pressure, which on the whole should have a distinctly bene- 
ficial effect. 3 Altitude has a more pronounced effed upon hyper- 
tension due to genera] arteriosclerosis than upon that associated 
with well-marked nephritic lesions- (see page 53). 

The question as to the effect of altitude upon the individual is 
an important and practical one. The physician is constantly con- 
sulted regarding the effects of high altitude in tuberculosis, heart 
disease, emphysema, etc. It is generally agreed thai residence 
at a high elevation increases the number of erythrocytes and the 
percentage of hemoglobin. There is also reason to believe that 
the cells of the pulmonary alveoli possess and may take on an 
increased capacity to secrete oxygen into the blood. These changes 
are of a compensatory nature. 

Plungian's investigations indicate thai barometric changes at 
a given altitude exercise an effect upon individual blood-pressure, 
although this is inconstant, both quantitatively and qualitatively. 
The most marked changes generally occur in tuberculous and 
arteriosclerotic subjects after a sudden fall of the barometer. 

The Effects of Tropical Climate. Much has Keen written on 
the effects of tropical sunlight on white men. To whatever the 
deleterious effects are due, they are apparently not the result of 
blood-pressure changes, due average blood-pressure of Americans 
in the Philippines is somewhat lower than that when at home. The 
lowest readings are obtained during the first three months of tropical 
residence and during the hottest months. No difference has been 
noted among individuals with light or dark complexions, nor when 
different types of underwear are worn. 4 In a study of 717 Filipinos 
made by Conception and Bulatao 5 it was found that in individuals 
averaging 28.5 years the average pressure for men was * \ 5 q 5 , for 

1 Peters and Bullock: Blood-pressure Studies in Tuberculosis at a High Altitude, 
Arcb. Int. Med., 1913, xii, 458. 

2 Schrumpf , P. : Blutdruckuntersuchungen u. Energometerstudien im Hochge- 
birge bei Herz- u. Kreislaufstorungen, Deutsch. Arch. f. klin. Med., 1914, xciii, 466. 

3 Plungian, M.: Ueber d. Wirkung athmosphaeriseher Einflusse auf d. Blutdruck, 
Dissert. Basel, 1913, p. 43. 

4 Chamberlain, W. P. : A Study of the Systolic Blood-pressure and the Pulse 
Rate of Healthy Adult Males in the Philippines, Philippine Jour. Sc, 1912, vi, 467. 

6 Conception, I., and Bulatao, E. : Blood-pressure Picture of the Filipinos, 
Philippine Jour. Sc, Sec. B., Trop. Med., 1916, ii, 135. 



376 METABOLIC DISEASES AND MISCELLANEOUS CONDITIONS 

women ^fjp, with a pulse-pressure of 36 and 33 mm., respectively. 
This is distinctly lower than the usual pressure of the white races 
in temperate zones but similar to that found among whites residing 
in the tropics. This lowered pressure has been ascribed to dim- 
inished resistance in the arterioles together with increased activity 
of the sweat glands. According to McCay the pressure of the 
natives of India is lower than that which obtains in western Europe, 
and yet arteriosclerosis is very common among them. Possibly the 
low protein diet and more constant perspiration may have a bearing 
upon the low pressure. Oliver's investigation showed that during 
prolonged hot weather blood-pressure was lowered in the brachial 
artery, but was increased in the phalangeal vessels. 1 

Life Insurance. — The importance of blood-pressure examinations 
as a means of sifting out undesirable "risks" has now become 
generally recognized by life insurance companies and is routinely 
required by many of them. Statistical studies have shown that 
blood-pressure values, abnormal in relation to the age and sex 
of the individual, are definitely associated with a shortened expec- 
tancy of life. It would seem that pressures of 20 mm. either below 
or above the normal standard require an explanation. As has 
been stated elsewhere, high pressures often indicate renal, and 
low pressures, tuberculous disease. 

Fisher 2 has pointed out that a pressure of 150 gives a higher 
mortality than an average risk, and an increase of 15 per cent, 
above the normal pressure for a given age should always excite 
suspicion. Among 2661 risks with an average pressure of 142.43, 
at the ages of forty to sixty, the mortality was about the same as 
the average general mortality of the company, but with an average 
pressure of 152.58 among 525 risks the mortality increased 30 per 
cent, in excess of the average. Among the rejected risks with an 
average pressure of 161.44 (1970 applicants) the mortality was 190 
per cent, of the medico-actuarial table and more than double the 
average mortality of the company. During the interval of from 
1907 to August 1, 1913, 1970 applicants were refused insurance 
solely on the basis of a pressure of 160 mm. Ilg. These cases but 
for the pressure readings would have been accepted. The con- 
tinued accumulation of life insurance statistics will throw much 

1 Quoted, Allbutt: Diseases of the Arteries, Including Angina Pectoris, London, 
1915, i, 181. 

2 The Diagnostic Value of the Sphygmomanometer in Examinations for Life 
[nsurance, Jour. Am. Med. Assn., 1914, lxiii, 1753. 






LIFE INSURANCE 377 

light not only upon the diastolic pressure and upon hypotension, 

but also on a large and important class of individuals who have only 

slightlj increased pressure, who consider themselves in perfed 
health and do not, therefore, come under tin- observation of the 
physician. 

As a ready means of calculating what u given individual's blood- 
pressure should be, Faugh.1 has suggested the following rule: Assume 
that the normal systolic pressure of a person aged twenty years 
is 120 nun., and add 1 mm. Hg. for each additional two years 
of life. 

The different phases of blood-pressure as applied to life insurance 
have been discussed in different chapters of this hook. The reader 
is specially referred to Instrumental Technic, page L29; Sources 
of Error, page L26; Physiological Variations with Special Reference 
to Age, page 50; Hypertension in Nephritis, page 276; Hypotension, 
page 193. 

Infants and Children. — Blood-pressure estimations in infancy 
and early childhood are made with difficulty and fraught with 
inaccuracy. The psychic effects produced by the procedure, which 
often result in crying or struggling, absolutely vitiate the accuracy 
of the readings. The arm is too small to permit satisfactory applica- 
tion of the cuff, hence the readings should he taken on the thigh 
and a small cuff (6.5 cm.) employed. As a temporary makeshift 
the usual 12 cm. cuff may be folded in half. The child will pay less 
attention to the cuff when it is applied to the lower extremity. 
The diaper must be loosened. Auscultation is more satisfactory 
than palpation. The diastolic pressure which is determinable with 
difficulty" owing to the small size of the artery and of the pulse- 
pressure, must generally be estimated either by auscultation or 
by means of a Fedde oscillometer or some similar device. In 
childhood and youth the transmission of the pressure wave from 
the centre to the periphery behaves differently than in the adult. 
In the former the systolic pressure in the digital artery equals 
that registered in the brachial, whereas in the adult, especially 
in cases of nephritis and arteriosclerosis, the arterioles are tonically 
contracted as well as less elastic, and the systolic brachial pressure 
is much higher than that in the digital arteries. 1 

The diastolic pressure is relatively higher and the pulse-pressure 



1 Findlay, L.: The Systolic Pressure at Different Points of the Circulation in the 
Child and the Adult, Quart. Jour. Med., 1910-11, iv, 489. 



378 METABOLIC DISEASES AND MISCELLANEOUS CONDITIONS 

is about 10 mm. less than in adults. 1 On the whole, blood-pressure 
estimations arc of much less value in children than in adults. 

Normal Pressure. — Before birth blood-pressure is higher in the 
pulmonic, than in the systemic circulation. The expansion of the 
lungs promptly lowers pulmonary blood-pressure. Before this 
occurrence most of the blood passes from the pulmonary artery 
through the ductus arteriosus into the aorta, but afterward, the 
lowering of hlood-pressnre which occurs in the systemic circulation 
when the placental circulation is cut off, causes a collapse of the 
ductus and thus favors its closure. Additional causative factors 
may he the equalization of pulmonary and aortic pressures and the 
muscularity of the ductus. (Abbott. 2 ) At birth systolic blood- 
pressure is said to range between 35 and 55 mm. Waking and 
suckling cause a rise of about 15 mm. 3 

Preceding the onset of puberty there is a tendency toward a 
fall of pressure, during pubescence there is a period of increased 
pressure which is in turn followed by a slight decrease after puberty 
has been established (Allbutt). (See Gonads.) The attempts which 
have generally been made to establish normal standards in relation 
to age have led to more or less confusion. Pressure increases with 
age, and during the first month of life the normal range lies between 
• ill and (is mm. llg. Some recent investigations have shown that 
blood-pressure increases with height and weight, and that these 
criteria are more definitely fixed than the mere age factor. 4 Further, 
the variations which have been attributed to the influence of sex 
are really dependent upon the effect of height and weight. 

Comparison of Bodily Height and Systolic Blood-pressure. 6 

Systolic 

blood-pressure. 
Height. Mm. 

3 feet 6 inches 99 

4 feet to 4 feel A inches 109 

4 feet 3 inches to 4 feet 6 inches 112 

4 feet inches to 4 feet 9 inches 118 

I feel '.i inches to 5 foot 120 

.") foot 125 

1 Melvin and Murray: Mood-pressure Kstinuition in Children, British Med. Jour., 
April 17, L915, i). 2833. 

'Congenital Cardiac Disease, ( >slcr and McCrae's Modern Med., 1915, iv, 111. 

1 Balard, 1'.: Le I'ouls el la Tension Arterielle do L'Enfant et du Nouveau-nc, 
Gu, dee Hop., L913, Ixxxvi, 837. 

i \\ olionsolm-Kriss: Ueber Blutdruck im Kindesalter, Arch. f. Kinderheilk., liii, 
Nos. 4 6. 

Michael, M.: A Study of Blood-pressure in Normal Children, Am. Jour. Dis. 
Child., Mil, i, 272. 



BLOOD-PRESSURE AND PHYSICAL EFFICIENCY 379 

Comparison op Weight and Blood-pressure. 

Blood i" - 

Weight, Mm. 

30 to 40 His 95 

10 to 50 " LOO 

50 to 00 " 1(17 

60 to 70 " L12 

70 to 80 " . 116 

80 to 90 " . . . 122 

'.in to LOO " 12G 

The foregoing tables explain the statement frequently made 
that "robust" children have higher pressures than delicate ones, 
and perhaps also that breast-fed infants give higher readings than 
those artificially nourished. Popoff 1 found the systolic and diastolic 
pressures in the newborn infant to average 7."> and :'. I nun. Hg. 
respectively. Prematurely born infants had lower pressures (see 
page 50). Laitao found that at the end of seven months the systolic 
pressure was generally 100 nun., and that the pulse-pressure which 
during the first month averaged 18 nun., at the end of the first 
year hail reached 28 nun.- These values are higher than those 
obtained by Kaupe, 3 who found an average pulse-pressure of 8 to 
10 mm. Hg. 

In infants after feeding the pressure is increased 8 to in mm., 
and during sleep pressure ranges between (ill and 70 nun. In 
children an hour's exercise may elevate the pressure 5 to 1" nun., 
at which point it may remain for half an hour (Trumpp) (see also 
Acute Infections, page 204). 

Blood-pressure and Physical Efficiency.— Studied from the 
stand-point of the "Intercollegiate Standard," which consists of an 
addition of the strength of the back, plus that of the legs, plus that 
of the right and left forearms, plus the lung capacity divided by 20, 
plus bodily weight divided by 10 and the multiplication of* the last 
figure by number of times the subject is able to dip his body by 
the strength of his arms and shoulders, Barach and Marks found 
that there is no constant relation between physical efficiency (which 
also means circulatory efficiency), and either the pulse-pressure, 
diastolic pressure ratio, nor between the pulse-pressure percentage 
of the diastolic pressure. 



1 Beitrag z. Frage nach d. Blutdruck b. gesunden Kindern, Dissert. St. Peters- 
burg, 1913, p. 200. 

2 Laitao, M.: Pression Arterielle chez l'enfant. Arch. d. Mai. d. Enfants, 1913, 
xvi, 102. 

3 Der Blutdruck im Kindesalter, Mcnatsschr. f. Kinderheilk., 1910, ix, 257. 



380 METABOLIC DISEASES AND MISCELLANEOUS CONDITIONS 

The following tables compiled by Barach and Marks 1 show the 
actual systolic and diastolic pressures encountered among 742 
male students: 



Age Distribution in a Series of 552 Consecutive Cases. 

Age, Years. Cases. 

15 to 17 27 

17 to 19 200 

19 to 21 202 

21 to 23 71 

23 to 25 "31 

25 to 27 12 

27 to 29 6 

29 to 31 1 

Over 31 2 

Total 552 



DlSTRIIiUTION OF MAXIMUM PRESSURE IN 656 CASES. 

Mm. Hg. Cases 

90 to 100 7 

100 to 110 23 

110 to 120 112 

120 to 130 204 

130 to 140 153 

140 to 150 95 

150 to 160 45 

100 to 170 14 

170 to 180 ) 

180 to 190 | 3 

190 to 200 J 

Total 656 



Minimum Pressure Read at the Last Clear Sound. 



Cases 

11 

4 

12 

41 

94 

90 to 100 121 

100 to 110 27 

L10 to 120 9 

120 to 130 . . 3 



Mm. Hg. 


40 to 


50 


50 to 


60 


60 to 


70 


70 to 


80 


80 to 


90 



1'/ 3 cases or 87 per 
cent. 



Total 312 



1 Blood-pressures: Their Relation to Each Other and to Physical Efficiency, Arch. 
Int. Med., 1914, xiii, 648. 



BLOOD-PRESSURE \\l> PHYSICAL EFFICIENCY 38] 



I 

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101.0 96.0 
119 2 71 2 
106.167.4 


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70.2 




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: S3 £ 


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CJWOCT US ^jO"° 


i 


Palpation 
Palpation 

Erlangcr 

Palpation 

Ausoultation dias- 
tolic, 5 I'has. 

Auscultation dias- 
tolic, 5 Phas. 

Modified Erlanger 






1 

3 


Gordon (L.) . . 
Stowcll 

Laitao (M.) . . 
K'aupc (W.) . . 
Kriss (W.) . . 

Katzenberger (A.) 

Judson and 
Nicholson . . 



O — — -H 



1 1 III 



382 METABOLIC DISEASES AND MISCELLANEOUS CONDITIONS 

The foregoing tables are taken from Judson and Nicholson, 1 

who include their own figures based upon a study of 2300 children. 
As these authors point out, "The widest variations occur from the 
tenth to the fourteenth year when there is a marked rise in the 
systolic pressure. From the fourth to the fourteenth year, inclusive, 
the variations do not exceed 5 mm. in two-thirds of the cases.'* 
Their systolic readings were higher than those previously obtained 
by others. There is a gradual rise of pressure as age increases 
between the ages studied, amounting in all to 14 mm. Ilg. Up to 
eight years of age a 9 cm. cuff gives accurate readings, but after 
eight years a 13 cm. armlet should be employed. The onset of the 
fourth auscultatory phase (muffling) must be used as the diastolic 
criterion. 

Athletics. — The physician is frequently consulted regarding the 
advisability of allowing certain individuals with functional or 
organic heart lesions to indulge in athletic exercises. The tendency 
at present is certainly to be more liberal in what may be allowed 
than was formerly the case. This is specially true of children and 
young adults with heart murmurs. Before assenting to or advising 
such procedures, however, we must realize that although exercise 
is as necessary for the heart as for any other muscle, yet certain 
forms of exercise throw an enormous burden upon the circulatory 
apparatus (see page 49). 

Any exercise which increases the pulse-rate will also in a normal 
individual raise blood-pressure. This results not only from the more 
rapid heart rate but also from an enlarged systolic output. 

After exercise blood-pressure falls below normal. This applies 
to all the pressures, but the systolic element falls more rapidly than 
the diastolic, and thus the volume of the pulse decreases. The more 
strenuous and exhausting the exercise the longer will pressure remain 
subnormal. After moderate exercise pressure remains low for about 
half an hour. After a sudden sprint of one hundred yards it may re- 
quire three times as long before the normal level is reached. I .owsley- 
snggests that when the subnormal phase is overcome in the space of 
an hour, the exercise may be considered well within the hygienic 
limits for the individual, but that a depression lasting two hours 
should be regarded as excessive. 

The more sudden and violent the exercise (sprinting, hammer 
throwing, etc.)j the greater the rise of blood-pressure (2(H) mm.) 

i Blood-pressure in Normal Children, Am. Jour. Dis. Child., 1914, xii, 257. 
2 The Effects of Various Forms of Bxercise in Systolic, Diastolic and Pulse-pressures 
and Pulse Elate, Am. Jour. Physiol., 1910-11, xxvii, 446. 



EFFECT OF MARATHON RACES 383 

and the more rapid the pulse. Endurance exercises (long distance 
running, etc.), produce a more gradual and less extreme rise of 
pressure, but a pressure which remains high for a longer time. The 
sudden changes of pressure in the former group probably do no 
harm to young normal individuals with resilienl arteries, but they 
should be avoided by elderly men in whom permanent cardiac 
dilatation may result. The prolonged strain of endurance exercises 
among young growing children should certainly not he encouraged 
(McKenzie). 

The Effect of Marathon Races. Before the Race. Most of the 
men had trained for six to nine months preceding the race of twenty- 
four miles. The majority showed evidences of cardiac enlarge- 
ment and had a slower pulse rate than normal. The cases which 
showed a more than average diurnal pulse variation also showed a 
cardiac hypertrophy and an increased blood-pressure. The bighesl 
blood-pressures wen 1 found in coincidence with the largest hearts. 
The men who had heart murmurs had even larger hearts and bigher 
pressures. As one would expect the men who were overweight, 
whose occupations were laborious, and whose periods of preliminary 
training were short, showed higher than average cardiac enlarge- 
ment and blood-pressures. 

After the Race. — The average fall of blood-pressure was 20 nun. 
Cases with heart murmurs showed an even greater drop. Some 
cases showed marked cardiac dilatation (rc-ray), and in these 
blood-pressure was lower than in those whose heart dilated less. 
At the end of six months both heart and blood-pressure examina- 
tions yielded normal findings in most of the cases but some increased 
much more slowly than others. 1 

If there is any doubt whatever regarding the organic character 
of a murmur it is better to err on the safe side and advise against 
prolonged or severe forms of athletics. 

Much has been written of late concerning the evil effects of over- 
athleticism, and regarding this subject there is much difference of 
opinion. 

Severe exercise of an hour has been shown to not infrequently 
cause the appearance of albumin, casts and blood cells in the urine 
of healthy subjects, phenomena which are doubtless due to circula- 
tory changes in the kidney at a time when waste products in large 
amount must be eliminated. 2 

1 Savage, W. L. : Physiological and Pathological Effects of Severe Exertion 
(The Marathon Race), Am. Phys. Educ. Rev., 1910, xv, No. 9; 1911, xvi, Nos. 1-5. 

2 Barach, J. H. : Against Overathleticism, Tr. IV Internat. Congress of School 
Hygiene, Buffalo, August, 1913. 



3S4 METABOLIC DISEASES Ah D M TSt ELLANEOUSCONDITIOXS 

Prolonged and severe athletic training produces demonstrable 
cardiac hypertrophy with increased blood-pressure. These phe- 
nomena maj be transient and ephemeral, but they are not 

always so. . 

It certainly does uo1 seem reasonable to believe that Marathon 
races run by poorly developed and untrained individuals, as we 
see them in our city streets, can be beneficial. Nor does it seem 

I ical to assume that four-mile boat races at the end of which even 

trained athletes go into a state of syncope, can be considered 
healthful exercise. It is believed by some that strenuous athletics 
use up an individual's reserve force -his vital reserve. Whether 
tins be so or not cannot be proved, but certainly the picture of the 
husky giant who succumbs in the early stages of typhoid fever or 
pneumonia is an all too common one. 

It is very questionable whether in the ordinary course of lite, 
the " athletic heart" is an asset. Investigations among the athletes 
at the University of Wisconsin have shown cardiac abnormalities 
among a considerable proportion of the athletes. 1 This has been 
attributed by some apologists to faulty methods of training. The 
report of the Surgeon-General of the United States Navy attributes 
a large excess of deaths attributable to cardiac overstrain among 
the cadets of Annapolis, to overathleticism. In cardiac cases the 
physician carefully questions the patient regarding antecedent infec- 
tions, but rarely in regard to athletic overindulgence or mishaps. ^ 

It seems merely conservative, therefore, to insist that competitive 
athletics should be conducted only under competent medical 
supervision, and that growing boys should not be allowed to indulge 
in the prolonged and exhausting competitions which greatly tax 
even a fully developed heart. 

r,lood-pressure observations made upon men carrying the regular 
soldier's equipment of the German army during an endurance 
march, .bowed in those between the ages of eighteen and twenty-five 
a Fall of L2 mm.; under eighteen years it was \\) mm., and in older 
„,,,, averaged 38 nun. Kg. 2 The stress and strain of the present 
war according to Moutier is accountable for many cases of hypo- 
tension. Even hypertensive individuals are said sometimes to 
return on furlough with a normal pressure. He also reports variable 
tension in the two arms when one has been injured, sometimes 
higher but generally lower in the traumatized member. 

i Schumacher, L., and Middleton, W. S.: The Cardiac Effects of Immoderate 
College kthleticB, Jour. Am. Med. Assn., 1914, lxii, 1136. • 

Le: Aerztliche Beobachtungen an Teilnehmer ernes Armee-GeiKu-.ksnars, h. a, 
Deutsch. med. Wchnschr., L915, xli, 1425. 



BLOOD-PRESSURE IN G ASTRO-ENTERITIS 385 

The Effect of Athletic Training.— Training renders an individual 
more efficient (1) by increasing cardiac and vasomotor responses 
to meet sudden or prolonged demands for physiological activity; 

(2) by educating the brain centres so that muscular actions bee 

semi-automatic and hence less volition is required in their perform- 
ance; (3) by accustoming the medullary centres to an increased 
quantity of carbon dioxide; and (4) by Increasing the rate of 
excretion of waste products of metabolic activity. 

Middleton 1 has found that training during a football season 
produces fairly uniform results which may be expressed ;is follows: 

1. A proportionate decrease in both systolic and diastolic pressure 
during the training period. 

2. After the rest following the training season a rise of both 
pressures occurs which exceeds the anteseason records. 

3. The blood-pressure reaction to a test of fifty stationary run- 
ning steps is practically unaltered by the training. 

The decrease in the blood-pressure mentioned may be due to 
peripheral vascular relaxation or to cardiac dilatation, or to a com- 
bination of both factors. 

Blood-pressure in Gastro-enteritis. — The suggestion lias been 
made that the collapse which occurs in the course of epidemic 
diarrheas is in part due to a fall of blood-pressure resulting from 
loss of fluid in the tissues thus producing anuria, and that saline 
infusion should be used in combating this symptom 2 (see Cholera, 
page 207). 

Vomiting causes a fall of blood-pressure which is in part due to 
the cardiac inhibition which occurs when the vomiting centre is 
stimulated 3 not only a fall, however, but very sudden and extensive 
pressure variations are also met with. 4 

1 The Influence of Athletic Training on Blood-pressure, Am. Jour. Med. Sc, 1915, 
cl, 426. 

2 British Jour. Child. Dis., 1912, ix, 343. 

3 Miller: Am. Jour. Physiol., May, 1915. 

4 Brooks and Luckhardt: Blood-pressure during Vomiting, Am. Jour. Physiol., 
1915, xxxvi, 104. 



25 



CHAPTER XVI. 

DISEASES OF THE NERVOUS SYSTEM. 

Neurasthenia.— When we consider what a large number of dif- 
ferent organic and functional abnormalities go to make up the 
clinical picture of this condition it is not surprising to note that 
blood-pressure Endings are inconstant. As has been described 
elsewhere, many of these cases belong in the category of "con- 
stitutional low arterial pressure" {q. v.), but some cases have been 
reported as associated with hypertension. Symptomatic improve- 
ment is generally attended by the reestablisbment of a more normal 
pressure, whether this means a rise or fall. 1 "Neurasthenia" 
associated with high blood-pressure generally calls for a revisbn of 
diagnosis, which will not infrequently be changed to nephritis or 
cardiovascular hypertensive disease. 

- In true neurasthenia, in real exhaustion of the nervous centres 
from whatever cause arising, the blood-pressure is low, lower than 
in any other chronic malady, except the terminal phases of cancer 
tubercle and other wasting disease" (Leonard Williams). The 
effects of prolonged mental and physical strain and exhaustion, 
as exemplified by soldiers returning from the battle front in France, 
produces arterial hypotension. Moutier reports that a well-marked 
fall in pressure occurs both in soldiers starting out with normal 
pressures and in those who do so with hypertension. 

Neuroses, etc.— In the neuroses unequal radial pressure on the 
two sides is often found as well as a general lability of pressure. 
These signs may be of use in diagnosticating between neurosis and 
simulation. 2 Pain produces a rise of blood-pressure and an increased 
pulse rate. Simulated pain does not. This fact has been turned 
to practical application in the detection of malingering in relation 
to industrial insurance. In persons with normal sensibility the 
blood-pressure under the application of faradic stimulation to the 
upper thigh rises from 8 to L5 mm. In organic affections of the 

iMacnainara: Lancet, July 18, 1908. .... 

■ Sand: I.- Anomalies de la Tension, Sanguine, etc., Arch, intern, de Med. 

Legale, Ulin, p. 349. 



\ i i:\t\i. disease 387 

spinal cord, multiple sclerosis, hysteria, etc., it remains unaffected 
when stimulation is applied to analgesic regions. 1 

11' the systolic pressure is taken in one arm and limultaneously 
die diastolic pressure in the other (for celerity of procedure, and 
the subject is emotionally disturbed by conversation, gesture, or 
the application of ice to the abdomen, (1) marked variations of 
the maximum pressure are said to indicate abnormal stimulability; 
(2) if the diastolic pressure meanwhile remains unaltered the 
vascular system is normal; (3) if the diastolic pressure shows 
sudden variations of over 15 per cent, of the systolic pressure we 
are dealing with arteriocapillary sclerosis.' 2 Landerer found abnor- 
mal arteriocapillary pressure relations in neuroses. 

Peripheral Neuritis. — In the early stages of brachial neuritis, 
Stewart found the blood flow greater than in the unaffected hand, 
a finding which he interpreted as indicating a partial paralysis of the 
vasoconstrictor fibers in the nerves involved. 

In neuritis affecting chiefly the muscular nerves, disturbances 
of the blood How were less conspicuous than when the cutaneous 
nerves were involved. This is presumably due to the fad that a 
large amount of the total blood supply of the extremities traverses 
the skin of the parts. 

Cases of long-standing unilateral neuritis were found by Stewart 

to show a diminished bl 1 How on the side affected, owing either 

to diminution of the arterial lumen following injury of the vasomotor 
nerves or perhaps to an adaptive correlation between diminished 
function and blood supply. 

Mental Disease. — The reports on blood-pressure in abnormal 
psychic states are so variable and contradictory, and the range of 
abnormality so slight, that one cannot but feel that in the majority 
of cases at least no definite relationship exists. Nor is this surprising 
when we consider how greatly blood-pressure is normally affected 
by emotional disturbances. 

In simple, acute, passive, and demonstrative melancholia high 
pressures have been reported, whereas chronic melancholia is 
associated with hypotension. Hawley states that cases of mania 
show definite and typical blood-pressure changes — a large pulse 
amplitude with sudden pulsatory oscillations and an increased 
pressure. These phenomena disappear when the mental state again 
becomes normal. In pure senile mania and melancholia the readings 

1 Curschmann : Deutsch. med. Wchnschr., October 15, 1907. 

2 Schrumpf and Zabel: Die diagnostische Bedeutung der psychogenen Labilitat 
des Blutdruckes, Munchen. med. Wchnschr., 1911, lviii, 1952. 



388 DISEASES OF THE NERVOUS SYSTEM 

correspond to those registered in the same states in earlier life. 
Senile dementia, characterized by restless fidgeting, etc., shows 

increased pressure. 1 In depressed and stuporous mental states 
low pressures are found. 2 

The vasomotor unrest of the insane has been corroborated by 
Enebuske 8 who makes the following observations after 20,000 
blood-pressure estimations. Characteristic of the manodepressite 
group is vasomotor unrest at a hypertensive level, continuous within 
certain periods of time. In other words, there are frequent pressure 
alterations with an average high level (150 mm.). The variability 
c jases after a time and when blood-pressure has become stabilized 
the disease has cither run its course or become altered. 

In the precox group continuous vasomotor unrest also occurs, 
but ;it a lower level. Pressure variations are more marked than in 
the manodepressive class, and the vasomotor unrest is continuous 
without a time limit through periods of remission with vasomotor 
tranquility (except for periodical precox). In all of the preceding 
forms, pressure levels vary during the acute and subacute stages. 
During the periods of vasomotor tranquility the patients are more 
responsive and receptive to treatment. 

Dementia Precox. — According to Perazzolo 4 74 per cent, of these 
cases have a low blood-pressure. Turner found no definite relation 
between blood -pressure and cither exalted or depressed mental 
stales. The height of the pressure seemed mainly dependent upon 
the age of the patient and upon the presence of renal or cardio- 
vascular complications. 5 

Epilepsy. -Epileptics not infrequently have a, slow pulse rate, 
a low blood-pressure, and evidences of peripheral stasis. Russell, 6 
in his Goulstonian lecture, enumerated many interesting and 
suggestive points in an analogy between epileptic seizures and 
vascular spasm. We cannot, however, assume that such conditions 
affect the cerebral vessels in the same manner as or simultaneously 
with the peripheral arteries. Furthermore, there is still some 
difference of opinion as to whether the cerebral vessels possess 
vasomotor nerves. Hut the clinical picture of epilepsy presents 

1 Alexander: Lancet, July 5, 1902. 

* Hawley: Blood-pressure in States of Excitement and Depression, Arch. Inl Med., 
1913, xii, 526. 

BoBton Med. and Sur^. Jour., March 15, 1917, No. 11. 
1 Revista sperimentale di Freniatria, April M0, 1909. 
r Tumor: Observations on the Blood-pressure and Vascular Disease in the Female 

Jour. Ment. Sr., 1909, riv, im 
■Some Disorders <>f tin- Cerebral Circulation and Their Clinical Manifestations, 
Lancet, April :'., L909, pp. 963, 1031, 1093. 



BRAIN TUMORS, HEMORRHAGES, AND MENINGITIS 389 

many features which fit well into a hypothesis of vasomotor crises 
(aura, [tailor, syncope, convulsions, etc.). 

Blood-pressure has been found to increase several hours before 
the attack begins. During the seizure it is said to rise still further 
(20 per cent.) and to fall after the attack; but often to remain 
somewhat elevated between paroxysms. 1 It has been shown thai 
in many cases rhythmic blood-pressure variations occur which 
are not due to respiratory movements (Traube-Hering waves). 
1* receding the seizure (twenty-six to sixty seconds' there is a rise 
of pressure (followed in some eases by a sudden fall), then apnea, 
and finally the convulsion.- The pulse is variable. "A study of 
the changes in the respiratory and circulatory systems in some 
of the cases of epilepsy suggests that the site of the discharge is 
in the medulla and pons I the 'lowest level of fits' of Hughlings 
Jackson). Likewise it points to the medulla as participating in 
the discharge in all cases of epilepsy whether this discharge originates 
them or not.'' 3 

Brain Tumors, Hemorrhages, Meningitis, etc. The increased 
intracranial tension which occurs in cases of apoplexy and brain 
tumor may be closely simulated experimentally. The symptoms 
of the two conditions as well as their mechanism is essentially 
similar. Sudden increase of intracranial tension produces an 
acute anemia of the brain, which, being enclosed within osseous 
confines, is relatively incompressible. The only possible relief 
from such compression can come through absorption of the cerebro- 
spinal fluid. If the rise in arterial tension is prevented death occurs 
from medullary anemia. 

With increasing compression the following symptoms generally 
occur in the order mentioned: (1) unconsciousness; (2) respiratory 
abnormalities; (3) increased arterial tension with bradycardia; (4) 
hypotension, tachycardia, death. Associated with these symptoms 
rhythmic fluctuations of blood-pressure (Traube-Hering waves) and 
Cheyne-Stokes respiration are apt to occur (see pages 43 and 300). 

The attendant rise of systemic blood-pressure is therefore com- 
pensatory: an effort to prevent medullary anemia, which if pre- 
vented causes death. The symptoms which arise are for the most 

1 Lallemand and Rodiet: Des Modifications de la tension arterielle chez les epi- 
leptiques L'Encephale, iv, No. 11. 

2 Gibson, Good, and Penny: The Pulse Immediately Preceding the Epileptic 
Attack, Quart. Jour. Med., 1910, iv, 1. The authors could find no alteration of 
the pulse amplitude up to the point of the seizure. 

3 Pollock and Treadway: A Study of the Respiration and Circulation in Epilepsy, 
Arch. Int. Med., 1913, xi, 445. 



:;«•«» DISEASES OF THE NERVOUS SYSTEM 

part due not directly to pressure but to cerebral anemia. When 
intracranial pressure becomes sufficiently great certain symptoms 
and signs become apparent (headache, vertigo, vomiting, choked 
disk, etc.). If pressure is increased still further, bulbar symptoms 
develop: bradycardia, hypertension. Finally, if anemia threatens 
the vital centres life can only be maintained by a marked rise of 
general blood-pressure, and this at least intermittently usually 
occurs. Some of the highest blood-pressure readings on record 
(300 iiiui.-H have been encountered under these conditions. 
Eventually, unless the pressure is relieved, death occurs as a result 
of central and systemic exhaustion, preceded by a fall of tension 
and an increased pulse rate (see page 45). 

Any increase of the cerebrospinal pressure, whether due to tumor, 
softening, hemorrhagic meningitis, cerebral or cerebrospinal menin- 
gitis (serous or purulent) tends to cause a rise of systemic blood- 
pressure. Especially is this the case if the pressure is exerted in the 
posterior cerebral fossa, causing a stimulation of the vasoconstrictor 
centre, and if the rise of intracranial pressure be rapid, lira in 
tumors are usually slow ingrowth and arterial hypertension, brady- 
cardia and respiratory disturbances are not marked unless a sud- 
den increase of intracranial tension occurs — hemorrhage, edema or 
ventricular effusion (rushing). 

If the cerebrospinal pressure is relieved by lumbar puncture or 
trephining, blood-pressure falls, the bradycardia is replaced by 
a normal pulse rate and respiratory abnormalities disappear. 
There is often a distinct parallelism between the two pressures. 1 

From what has been stated it is evident that phlebotomy is 
generally contra-indicated in cases of cerebral hemorrhage. On the 
other hand, a progressively rising arterial pressure is often the most 
useful indication of an increase of hemorrhage 1 and of consequent 
cerebral compression, and may therefore be used as a criterion as 
to whether an operation for decompression is or is not warranted. 

Apoplexy. —Marked hypertension is unquestionably a predis-' 
posing and often the direct cause of apoplexy, but less than 15 per 
cent, of the cases having a pressure of or above 200 mm. die from this 
cause. Furthermore, apoplexy max- occur in patients whose pressure 
has never been recorded as being over 170 nun. Immediately after 
an apoplexy, bradycardia with very high blood-pressure is some- 
times seen. These symptoms result from increased intracranial 
pressure. The usual range of pressure "after a stroke" is between 

Pariaot, J.: Hypertension cephalo-rachnidienne ct pression arterielle, Compt. 
rend. Boc. de biol., L909, bevi, 939. 



HEMIPLEGIA 391 

L50 and 200 nun., but QormaJ pressures may be found, or higher 
pressures (300 mm.-f-) than are encountered in almost any other 
clinical condition. Hemorrhage into the anterior fossa is less ap1 
to raise blood-pressure than when it occurs in the posterior fossa, 
especially in proximity to the fourth ventricle. Briggs has reported 
a pressure of 400 mm. Hg. The value of pressure readings 
depends mainly upon a knowledge of the pressure which existed 
preceding the attack. It is more important to know the 
general trend of the pressure — whether upward or downward 
than actual figures. Thus a steadily rising pressure indicates 
cerebral compression and may call for decompression, whereas a 
steady fall points to vasomotor failure, which often leads to death. 
Blood-pressure readings may be of value in diagnosticating between 
apoplexy and embolism. High pressure is evidence in favor of the 
former, and low pressure, of the latter. It appears, however, that 
apoplexy, even when associated with hypertension and chronic 
nephritis, is more commonly due to thrombosis with cerebral 
softening than to actual vascular rupture. ( 'ertainly this has been 
the case at the Philadelphia General Hospital. This statement is 
borne out by Cadwalader's 1 investigations, from which it appears 
that many non-fatal hemiplegias are due to vascular obstruction 
and softening rather than to hemorrhage, which is much more apt 
to cause death. 

The importance of pressure exacerbations as induced by exercise 
in precipitating apoplexy has perhaps been overestimated, a con- 
siderable number of "strokes*' occurring while the patients are at 
rest if not actually asleep, although, theoretically, increased pressure 
would tend to favor apoplexy or embolism, and decreased pressure 
thrombosis. The statement has been made that in cases of hemi- 
plegia, due to thrombosis, the pulse is rapid, intermittent and of 
low tension, whereas hemorrhage produces hypertension and brady- 
cardia. This appears to be true in typical cases. Often even 
rapidly fatal cases of hemorrhage fail to show either of the last- 
named symptoms (Collins). 

Hemiplegia. — Pressure differences in corresponding extremities 
are not infrequently seen in cases of hemiplegia. Dana states that 
marked differences on the two sides of the body suggest involve- 
ment of the optic thalamus. 2 Stewart found an abolition of vascular 
reflexes in an old case of hemiplegia on the affected side (see page 

1 Comparison of the Onset and Character of Apoplexy Caused by Cerebral Hemor- 
rhage and by Vascular Occlusion, Jour. Am. Med. Assn., May 2, 1914, p. 1385. 

2 Dana: Jour. Am. Med. Assn., December 19, 1909. 



392 DISEASES OF THE NERVOUS SYSTEM 

246). "In hemiplegia there is, in general, a marked deficiency in 
the blood flow in the paralyzed members. Considerable differences, 
however, exist in different cases in this regard, and also in the extent 
to which the vasomotor reflexes from the normal to the paralyzed 
part are affected. Whether these differences depend at all on the 
position of the lesion or are associated with the duration and com- 
pleteness of the paralysis has not been determined. There is some 
evidence that reflex vasoconstriction is more easily produced in the 
paralyzed parts than reflex vasodilatation." 1 

It has been shown experimentally that in dogs and cats there 
is a limitable region of the cortex, irritation of which causes a 
blood-pressure increase that is not coextensive with the motor 
zone, but is in cats situated more anteriorly. Irritation of this 
zone is sure to cause splanchnic constriction. It has been sug- 
gested, but as yet not demonstrated, that the pressor effects of 
certain cortical regions are limited in their action to certain regions 
of the body. The occurrence of unilateral differences in temperature 
and edema in hemiplegia, when the secondary effects of muscular 
paralysis can be excluded, indicate that similar cortical pressor 
centres exist in man. 2 

Locomotor Ataxia. — The crises of locomotor ataxia have long 
been recognized as clinical manifestations of the disease. The 
etiological part taken by the sympathetic nerve was explained 
by Duchenne. Putnam suggested that lesions of the sympathetic 
nerve might, owing to their influence on the vasomotor system, 
account for certain secretory abnormalities. The importance of 
vascular spasm in the genesis of the crisis has been chiefly cham- 
pioned by Pal, who reported a number of cases in which the crises 
were associated with hypertension (in one case 240 mm. Ilg.) and 
who regards the abdominal cramps as resulting from a spasm of 
the splanchnic arterioles, and a stretching of the nerve plexuses of 
the arterial wall. The attacks are sometimes relieved by nitrite 
of amyl. The rise of pressure occurs somewhat before the onset 
of pain, which begins when a certain variable high point is reached. 
The arteries become tense and the pulse rate increased. The 
pressure increase generally amounts to more than 50 per cent. 

licit/, and Norero 3 believe that the rise of pressure is the result 
of /in iii which they explain is due to a paroxysmal irritation of 

1 Stewart, (1. N.: Blood Flow in the Hands and Feet in Certain Diseases of the 
Nervou Sj item, \nh. Int. Med., 1915. xvi, 270. 

I Lewandowsky, W., and Weber, E.: Blutdruck u. Himrinde, Med. Klinik, 
L908, ii, 385. 

3 De la preasion arterielle chez les tabetiques, Arch. d. mal. du c<eur, 1908, i, 505. 



SYRINGOMYELIA 393 

tlu- posterior roots, and which is accompanied by local reflex 
phenomena in the corresponding segments; either (1) motor 
(vomiting, constipation) or (2) vasoconstrictor (hypertension). A 
rise of pressure is often absent in old cases owing to degeneration 
of the posterior roots, especially if chronic hypertension is associated. 
In opposition to Pal they failed to find arterial hypertension in cases 
of peripheral crises, although in most of their eases the disease was 
advanced. Stewart found the rate of blood flow in both hands and 
feet diminished in tabes; together with feeble vasomotor reflexes. 

It has been suggested that pressure readings might be of diag- 
nostic value in differentiating between tab. tie crises and biliary 
or renal colic since much higher readings occur in the former. 1 

Paresis. — The early observations of blood-pressure in paresis 
made by Pilcz and Alexander showed hypotension. Craig found 
the tension high during mental depression ami low during exaltation. 
The more recent studies of Walton 2 indicate that the average 
pressure in paresis is high, due doubtless to arteriosclerotic accom- 
paniments. When cardiac and renal diseases are excluded the 
pressure is slightly lower than normal. Such hypotension is, 
however, neither sufficiently great nor constant to be of diagnostic 
or prognostic value. The excited states are associated with variable 
pressures, but depression is more often accompanied by high than by 
low pressures. Toward the termination of the disease very marked 
hypotension may occur. 

Syringomyelia. — In a case of syringomyelia thermic stimulation 
of the affected arm produced no reaction in its fellow, whereas 
similar stimulation of the unaffected side arm produced a normal 
reaction on the diseased opposite side. These findings have been 
construed as showing that sensible stimuli occur in the "anti- 
dromal direction" after the manner of an axon reflex and produce 
a vasodilatation. 3 

1 Jump, H. D. : Value of Blood-pressure Estimations in Internal Medicine, Internal. 
Clinics, Series 21, i, 49. 

2 The Blood-pressure in Paresis, Jour. Am. Med. Assn., 1906, xlviii, 1341. 

3 Hess, L., and v. Bergmann, E.: Ueber Gefaessreflexe, Wien. klin. Wchnschr., 
1913, xxvi, 1297. 



CHAPTER XVII. 
BLOOD-PRESSURE IN SURGERY AND OBSTETRICS. 

The Effects of Hemorrhage. When an artery of large size is 
torn or cut and the resultant hemorrhage is considerable, the 
diastolic pressure falls, as does also the systolic pressure, although 
to a lesser degree. The pulse-pressure therefore increases and the 
left ventricle continues its normal output. Peripheral venous 
flow is. however, promptly reduced and soon the fall in venous 
pressure fails to supply an "effective" right auricular pressure. 
As a result of inadequate filling of the right heart, pressure falls 
in the pulmonary artery and in the left auricle, and systolic left 
ventricular output promptly falls. The medullary centres are 
stimulated by the decreased blood Mow, the pulse rate rises from 
depression of the cardio-inhibitory centre and vasoconstriction 
results from central stimulation. In addition to this mechanical 
factor chemical changes also produce their effects. The loss of 
erythrocytes from the blood stream with its consequent reduction 
in the oxygen-carrying power of the blood, together with a slug- 
gish circulation in the peripheral capillaries, leads to a decrease in 
the volume per cent, of oxygen in first the venous, and later, the 
arterial blood, while the carbon-dioxide content of each remains 
unchanged. This reduction in the hematogenous oxygen content 
causes hyperpnea, which causes for the time being a better average 
auricular pressure. In brief, "the fall of arterial pressures is 
counteracted by the augmented breathing, an accelerated heart, 
an accommodative contraction of the larger vessels and by per- 
ipheral constriction leading to an increased resistance and dimin- 
ished flow in spite of the reduction of viscosity." 1 

When hemorrhage ceases the loss of the blood bulk is made up 
by the absorption of lymph from the tissues. The rise of blood- 
pressure which results may be abetted by intravenous saline or 
salo-alkaline infusion. There appears to be no experimental evidence 
supporting the view generally held that active secondary, post- 
hemorrhagic vasoconstriction plays much of a part in this post- 
hemorrhagic rise of the mean pressure. 2 

The consecutive changes occurring during hemorrhage are 
represented in the following schemas taken from Wiggers's article. 

1 WinK'-rs, ('. .1.: Modern Aspects of the Circulation in Health and Disease, 
Philadelphia, I'M.-,, p. :«'.». 

'-' Wiggers, C. J.: Pathological Physiology of the Circulation during Hemorrhage, 
Arch. Int. Med., 1914, xiv, 33. 



THE EFFECTS OF HEMORRHAGE 



395 



SEQUENCE OF EVENTS DURING HEMORRHAGE. 
Reduction in Total Volume of Blood. 



Reduction in red cells and 
percentage of hemoglobin 



Venous blood-C02 unchanged 

decreased 

Arterial blood-C02 increased 

O2 decreased 



Stream slowed in tissues 

I 

Osmosis toward blood stream 

I 

Increase in volume 



Reduction in total arterial resistance 

I 
Decreased diastolic pressure 

1 
Increased systolic discharge of heal 

1 
Lower systolic, increased pulse-pressure 

Decreased flow in peripheral veins 

Decreased right auricular pressure 

Decreased output of right ventricle 

Decreased pulmonary arterial pressure 
and left auricular pressure 

Decreased output of left ventricle 

1 
Smaller pulse-pressure 

Further fall in systolic and diastolic press- 
ures 



Decreased flow through medulla 

y 1 \ 

• — — . 1 \ 

Stimulate Stimulates Depresses 

respiratory centre vasomotor card.-inhib. 

(deeper respirations) centre centre 

\ 1 / 
Reductions of red cells by Tend to counteract fall of pressure 
dilution of blood 

I \ / 

Decreased viscosity Tend to increase flow through small vessels 

SEQUENCE OF EVENTS DURING TERMINAL STAGES. 

Loss of Blood Volume Exceeds Resorption of Lymph. 

Red corpuscles reduced to minimum 



/ 
Oxygen percentage in arterial \ 
blood decreases 



Progressive increase in CO2 



\ 
Systolic discharge diminishes due to lack 
of diastolic filling 
i 
Pulse-pressure progressively diminished 
\ I 

^Respiratory centre depressed 
I 
Heart depressed by anemia 

i 
Beats slower. Feebler 

1 
Respiratory periodic gasps 

Asphyxial conditions 

Heart slow, large amplitude of contraction 

I 
Ventricular fibrillation, cessation 



396 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

IU l-pressure readings should be made in all cases in which 

anesthetics or surgical procedures are employed before, if possible 
during, and after the operation. Arterial hypertension will often 
indicate the presence of renal disease when the routine urine exami- 
nation fails to reveal it. A fall of pressure during the course of the 
operation is one of the surest methods of detecting the beginning 
of shock, whether this occurs during or after the conclusion of the 
operation. .1 fall of pressure In below 100 win. Hg., tot/ether with 
a rising pidsi rati-, is an indication for immediate treatment. Shock 
is at hand when the pulse-pressure falls to 10 to 15 mm., or when the 
diastolic pressure falls to or below 70 mm. Hg. (McKesson). When 
possible the patient's normal pressure should be obtained the day 
before the operation, or at least not immediately preceding it, 
because fear and excitement both tend to increase the systolic 
pressure and the pulse rate. A steady pressure is the best indication 
of a satisfactory condition on the part of the patient. Fluctuations 
of tension point to exhaustion. Patients with marked hypertension 
(180 to 210 mm. Hg.) require special care. The possibility of 
apoplexy, uremia, or heart failure must be borne in mind, and yet 
such patients not infrequently make perfect recoveries. Blood- 
pressure readings alone cannot be used as a criterion of safety; the 
patient's general condition must be carefully considered. Cases 
of arterial hypotension, especially if this condition is associated 
with lymphocytosis and other evidences of status lymphaticus, 
withstand anesthesia as badly as they do infectious disease. 

"Tin- practical surgeon should have knowledge of the following 
data: The effect of the general narcotic on blood-pressure and its 
relation to shock; whether in certain operations shock is less if 
the operation is carried on under spinal or local anesthesia, the 
effect of hemorrhage, the duration of the operation, exposure of 
the tissues to the air, effects of extreme heat or cold, the effect of 
manipulation or injury in various tissues or organs" (Bloodgood). 
While the manipulation of sensitive organs causes a primary rise 
of pressure, such a procedure may go far toward exhausting the 
\ asomotor centre. 

Surgical Shock. —Surgical shock- has been described as "a state 
of genera] apathy, reduced sensibility, extreme motor weakness, 
greal pallor, very small pulse, thready soft arteries, irregular gasping 
respirations, and subnormal temperature." 1 There is perhaps no 
subject in the whole domain of surgery regarding the pathology 
of which more radical differences of opinion exist than shock. 

■ Melteer, B. J.: The Nature of Shock, Arch. Int. Med., July, 1908, p. 571. 



SURGICAL shock 397 

This is at least in part due to the fad the term shock is applied to 
various conditions which may arise from trauma, intoxications, 
hemorrhage, etc. It has been suggested (Mann) that the term 
"shock" (similarly to the much abused and too inclusive term of 
"rheumatism" should be dropped, or if used at all, be limited to a 

condition in which without demonstrable he "rhage the amount 

of circulating Huid has been greatly diminished owing to venous or 
capillary stasis, or to exudation of serum or the diapedesis of 
corpuscles. 

Since the publication of Crile's work on blood-pressure in relation 
to surgical shock, the view that this condition is the result of an 
exhaustion of the vasomotor centres has been widely accepted. Crile 
originally stated that "neither the heart muscle, nor the cardiac 
centres, nor the respiratory centre, are other than secondarily 
involved." 1 Colla pse is due to a suspension of the function of the 
cardiac or of the vasomotor mechanism or to hemorrhage. These 
statements are based upon investigations of a large amount of clin- 
ical and experimental material which seemed to show that (1) the 
only constant finding in cases of -hock was a fall of blood-pressure; 
(2) there were no constanl demonstrable lesions in the circulatory 
apparatus; (3) the fall of pressure was no1 due to exhaustion of 
the peripheral nerve vascular mechanism; (4) that cocainization or 
destruction of the vasomotor centres produces a fall of pressure to 
the shock level ; (5) that drugs or other methods of treatment which 
raised arterial pressure were beneficial, whereas other stimulants 
which were employed were either useless or definitely detrimental. 
According to this hypothesis, then shock is due to an exhaustion 
of the vasomotor centre resulting from centripetal sensory stimuli. 

Muns 2 regards the symptom-complex, known as postoperative 
shock, as a combination of the effects of excitation and depression, 
which varies directly with the algebraic sum of these two factors, 
" The vasomotor centre is the variable factor in bringing about the 
vasomotor change; the variation of response is directly dependent 
upon the changes in the vasomotor centre produced by ether. 

In shock we find the diastolic pressure decreased, the pulse rate 
and the pulse-pressure increased. When cardiac exhaustion occurs 
the systolic pressure falls toward the diastolic level until the pulse- 
pressure becomes so small that the cardiac and respiratory centres 
are no longer sufficiently supplied with blood and death occurs. 

1 Crile, G. W.: Blood-pressure in Surgery, Philadelphia, 1903. 

2 Blood-pressure and Graphic Vasomotor Changes in the Periphery during Ether 
Anesthesia, Ann. Surg., 1916, lxiv, 645. 



308 BLOOD-PRESSURE TN SURGERY AND OBSTETRICS 

"A respiratory rate of more than 30 per minute is too rapid to 
assist in moving the blood, thus throwing the whole burden upon 
the heart" (McKesson). 

The experiments of Porter 1 and of Seelig and Joseph 2 have shown 
conclusively that the depression or fatigue of the vasomotor centre 
can no longer be considered as the primary cause of shock. Nor 
has it been demonstrated that the peripheral bloodvessels constantly 
or uniformly lose their tone. Mann 3 found that no amount of sensory 
stimulation would produce shock in the anesthetized animals so long 
as the abdomen is not opened and hemorrhage is prevented. 

Shock may he due to mechanical causes. The studies of Janeway 
and Jackson 1 showed that shock may he produced by partial, 
controllable occlusion of the inferior vena cava. The blood supply 
of the heart is thus diminished and arterial pressure falls. Even 
if the constriction is relieved and arterial pressure in part restored, 
death may later ensue in consequence of vascular changes — loss of 
tunc in the splanchnic capillaries and venules. According to this 
conception shock is a condition in which there has been a general 
displacement of a critical quantity of blood from the arterial to the 
capillary and venous portions of the circulation. 

( rile' believes that the essential lesions of shock are in the brain 
nils and are caused by the conversion of potential energy in the 
brain cells into kinetic energy at the expense of certain chemical 
compounds stored in the cells. As a result of certain noci impulses 
(fear, exhaustion, anesthesia., insomnia, etc.), the brain threshold is 
lowered and the trauma of operation or injury may produce the 
shock. In order to avoid shock it is necessary to exclude these noci 
impulses both of the special senses and of common sensation. The 
technic of anoci-association consists briefly in excluding all psychic 
stimuli by proper preoperative care of the patient, protecting the 
brain against destructive psychic strain during the operation by 
complete anesthesia and preventing nerve trauma by blocking the 
nerves with local anesthetics, ('rile lays the greatest stress on the 
psychic element, a conception which is not essentially at variance 
with Henderson's theory. 



1 'I' he Relation of Afferent Impulses to I lie Vasomotor Centres, Am. Jour. I'hysiol., 
L910, xxvii, 276; and The Vasotonic and Vasorefiex ( Yntre, ibid., 191"). xxxvi. 1 1 s 

\ i ocon brictoi ( entre during the Development of Shock, .lour. Lab. and Clin, 
Med., February 1 . 1916, No. •">. 

', in- Peripheral Origin of Shoek, Bull. .Johns Hopkins Hosp., 1914, xxv, 205. 
''Iln- Distribution of the Blood in Shock, Proc. Soc. Exp. Biol, and Med., 1916, 
xii. 19.:. 

»Tbe Kinetic Theory of Shock and its Prevention through Anoci-association 
(Shockless Operation), Lancet, July ■">, 1913, p. 7. 



SURGICAL SHOCK 399 

Yandell Henderson, 1 on the other hand, believes thai shock 
results from a lack of fluid in the circulation. According to this 
view there is a loss of CO2 from the blood (acapnia) which resuh 
from increased respiration due to pain, trauma, fever, acidosis, 
exposure of tissues, or maladministration of the anesthetic This 
causes a diminution of hemic osmotic tension, increased fluid 
transudation to the tissues, and a decrease in the total volume of 
blood. Owing to a fall of venous pressure the heart is no longer 
adequately filled with blood, and hence the systolic output dimin- 
ishes, and a, condition analogous to hemorrhage ensues. The experi- 
ments of Morison and Hooker- indicate that loss of ramus tone, 
causing a stagnation of blood in the veins and an insufficient filling 
of the right heart (as previously maintained by Henderson) plays 
a considerable part. Mann's investigations indicate that the loss 
of serum and erythrocytes caused by handling of the delicate 
vascular area of the splanchnics plays an important role. 

"The clinical signs of shock which appear after section of the 
abdomen and exposure of the viscera are due to a loss of circulatory 
fluid. This loss of fluid is not dependent upon any priuiar\ impair- 
ment of the medullary vasomotor centre and takes place at a point 
beyond the control of the vasomotor mechanism. The causes 
for this loss of fluid are apparently the same as those which deter- 
mine the accumulation of fluid in any other irritated area and pro- 
duce the signs of inflammation. The nervous system probably 
plays no greater part in the former case than in the latter. The 
condition is made grave when the viscera are exposed because of 
the great vascularity of the tissues involved." 3 

Corbett's 4 experiments led him to conclude that shock is of a 
composite nature, in which epinephrin exhaustion and oligemia are 
predominating factors, while anesthesia, pain, fright and trauma 
are immediate agents in producing epinephrin exhaustion as well 
as shock. Not "that epinephrin loss is shock, but rather epinephrin 
is necessary to overcome shock, and anything that depletes epi- 
nephrin favors the development of that condition." "Low blood- 
pressure is a constant accompaniment of shock, so constant, indeed, 
that investigators practically always express the state of shock 
in terms of manometric pressure." 5 

1 Am. Jour. Physiol., 1910, xxvii, 167. 

2 The Vascular Tone and Distribution of the Blood in Surgical Shock, Am. Jour. 
Physiol., 1915, xxxvii, 86. 

3 Mann, F. C: Shock and Hemorrhage: An Experimental Study, Surg., Gynec. 
and Obst., October, 1915, p. 430. 

4 The Suprarenal Gland in Shock, Jour. Am. Med. Assn., 1915, lxv, 380. 

5 Gray and Parsons: Anis and Gale Lectures, Royal College of Surgeons of 
London, March, 1912, British Med. Jour., April and May, 1912. 



400 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

W. T. Porter 1 who has recently made an extensive study of shock 
as seen in modern warfare, found that low blood-pressure paralysis 
and other abnormalities may result in men who are without 
visible wounds from the detonation of high explosives. In shock as 
seen in the trenches "there is no essential difference between the 
low pressure of men and that of other animals." When the diastolic 
pressure falls to 60 nun. or less shock is imminent, and when it 
reaches 1"> to 50 mm., recovery does not occur without aid. Accord- 
ing to Porter's observations one should prevent the occurrence of 
splanchnic stasis with its consequent disturbance of cardiac activity 
and nerve-cell nutrition by: (1) Placing the wounded in such a 
position thai the abdominal vessels will be higher than the heart and 
brain; (2) the application of heat; (3) intravenous saline infusion 
containing epinephrin; (4) blood transfusion in some cases, and 
(5) half-hourly observations of the diastolic pressure. Briscons 
and Mercier 2 state that (1) men knocked down by shell 
explosions have a rapid pulse and lower diastolic pressure similar 
to those visibly wounded. (2) Concussion alone accelerates the 
pulse but lowers the pressure far less. (3) Mere emotional stress, 
despite polypnea and other symptoms produces but little disturb- 
ance of either pulse or blood-pressure. 3 

In the early stages of shock a, marked rise of pressure often occurs 
as the result of stimuli which exert a vasoconstrictor influence", but 
owing to continuous stimulation of this kind a stage of depression 
occurs which may result in death. 

Hemorrhage is an important contributing factor in the produc- 
tion of shock, and all avoidable bleeding should be promptly 
checked. Sudden or large hemorrhage manifests itself by a fall of 
blood-pressure. A rapid and persistent fall of pressure with an 
increased pulse rate indicates a loss of blood too great for the 
organism to compensate for by peripheral vasoconstriction and by 
an additional expenditure of cardiac energy. The diastolic pressure 
is .mi index of far greater importance than the systolic, and a diastolic 
pressure of 50 mm. seems to be the lowest pressure at which the 
circulation can be maintained. (See Hemorrhage, p. 394. ) 4 Hough 

1 Shock at the Front. Boston Meet and Surj;. Jour., 1916, pp. 175, 854. 

4 Bull, de I'Acad. de Med., November 21, 1916. 

3 For a more detailed discussion of shuck sec Parham, F. W.: Shock, Its Nature 
and Management, South. Med. Jour., L913, vi, 763. Sec also J. M. Wainwright: 
The Present Status of Oui Knowledge of Shock, Penn. Med. Jour., December, 1914, 
p. lso. Gwathmey: Anesthesia, New York, 1911. Bloodgood, J. C: Prog. Med., 
1 December, 19] 1. 

• Balard, I'.: I. a Tension Lrterielle .Minimi Element de Prognostic des Bemor- 
rhagee Graves de la i ^rch. Mens. d'Obst. ei de Gyn., 1914, hi, 241. 



SURGICAL shock ID! 

manipulation, tearing of the (issues, especially when these have a 
large afferent nerve supply, s1 be avoided. "During the opera- 
tion the amounl of anesthetic should be as small as possible, the 
operation should be performed as quickly as is compatible \\ ith the 
safety of the patienl and the purpose of the intervention; tissues 
should be handled as gently as possible; if large nerves must be 
divided, as in amputations, they should be blocked with cocajn 
Injection; tissues should be exposed to air only when absolutely 
necessary; thej should be protected with warm, moist gauze; the 
patient should not be exposed to extremes of heat or cold. The 
weaker the patient to be subjected to operation, the more attention 
must be given to these details which lessen shock." 1 ( 'omplicating 
factors such as anemia, nephritis, diabetes, alcoholism, acute and 
chronic infections, metabolic disturbances, and psychic factors must 
also be borne in mind. 

The handling of tissues and organs supplied with sensory nerves 
by the cerebrospinal system is more apt to induce shock than i- 
the manipulation of those whose nerve supply is derived from the 
sympathetic nerves or the lower vagus. Furthermore, inflammation 
enhances the sensibility. Tumors are said to be insensible, but their 
connection with other tissues must be borne in mind. 

The Treatment of Shock. — The keynote of treatment lies in 
prevention which has already been considered. The arterioles and 
veins once they arc relaxed, do not readily regain the tonus. 1 fence 
the pressure required to keep up the circulation in the medulla and 
inthecoronaryarteriesmust.be produced by increased cardiac work. 
Drugs are for the most part unsatisfactory. 

The most rational therapeusis of shock consists in the slow and 
prolonged intravenous administration of pituitrin or epinephrin 
in normal salt solution. The amount of infusion necessary may be 
gauged by blood-pressure readings. Recent researches have shown 
that the intravenous administration of a molecular (8.4 per cent.) 
solution of sodium bicarbonate produces a marked rise of blood- 
pressure, an increased cardiac amplitude, and depth of respiration. 
These effects are due mainly to alkalinity, much less to bulk and 
hypertonicity, and in part to some other undetermined factor acting 
chiefly upon the heart, but not to the increased carbon dioxide 
content of the blood. 2 When the infusion of normal salt solution is 
employed in the treatment of shock due to hemorrhage, the amount 

1 Bloodgood, J. C: Surgical Shock, American Practice of Surgery, Bryant and 
Buck, 1906, i, 469. 

2 Selig, Tierney and Rodenbaugh: Jour. Am. Med. Assn., 1913, lx, 238. 

26 



402 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

of solution infused should be in excess of the amount of blood lost. 
In severe eases Downs' recommends 50 to 100 c.c. per kilogram of 
body weight. Infusion must not. however, be too rapid lest cardiac 
embarrassment result from right-sided hypertension. 8 

Heat loss must he prevented. Investigations have shown that 
in shocked animals camphor, administered intravenously, causes 
an actual fall of hlood-pressure. It is more apt to be efficacious 
when given subcutaneously. Strychnin likewise does not raise 
hi l-pressure, although it may be useful on account of its stim- 
ulation of the nerve centres. Nitroglycerin is definitely contra- 
indicated, although it may temporarily give a better color to the 
skin. Strophanthin intravenously increases pressure and is often 
useful. Caffein intravenously tends rather to lower than to raise 
blood-pressure. Airopin is often useful when the skin is clammy. 

In cases due to hemorrhage Ilogan" advises the intravenous 
infusion of colloidal gelatin. This solution, like blood serum, does 
not so readily escape from the bloodvessels as does ordinary salt 
solution. 

Inversion of the patient to increase blood-pressure in the brain 
should be tried, but not, of course, if the patient has already been 
in the Trendelenburg position. This posture may cause arrhythmia 
and, according to Pope, 4 even heart-block, "due either to acute 
dilatation, to toxins, or fatigue, or sepsis, or coronary clots, or 
direct trauma to some area of cardiac reflex." " It is quite possible, 
however, that from this position slight edema or exudate into the 
fourth ventricle may occur and may disturb the respiratory and 
pneumogastric centres. In shock from this cause Pope suggests 
venesection from the jugular vein, cardiac massage and epinephrin 
in Ringer's solution forced backward in the arterial stream, as 
giving the only possible chance for recovery." 5 Atropin, strychnin, 
or caffein in hypodermic administration are currently employed. 
The patient's head should he kept low, the feet elevated, the body 
warm and quiet. Blood-pressure may he elevated by bandaging 
the extremities, fresh air should be supplied and carbon dioxide 
in 6 per cent, concentration may be tried. 

According to Crile's anoci hypothesis, 6 stimulants are contra- 



i Am. .lour. Obst. and Dis. Women ami Child., 1916, lxxiii. 
• Simpson. V. !•'.: .lour. Am. Med. Assn., 1915, lxv, 941. 

: Intravenous Use of Colloidal (Gelatin) Solution in Shock, Jour. Am. Med. Assn. 
1915, p. 721. 

4 California Stale. lour. Med., December, 1913, p. 199. 

Edit. .lour. Aim. Med. Aran., 191 I, Ixii, 77(1. 
i (rile and Lower; Anooi-association, Philadelphia, 1914. 



SURGICAL SHOCK 103 

indicated, while morphin and other sedatives maj prove useful. 
Normal saline is beneficial temporarily and within limits, while 
human blood may be expected to \ ield the best results. All author- 
ities are agreed that preventive measures are of the greatest importance. 
Fear as usually encountered increases both pulse rate and blood- 
pressure, but in extreme degree blood-pressure may fall within a 
brief period as much as 60 mm. The elimination to the greatesl 
possible extent, of fear and anxiety on the part of the patienl before, 
and in preparation for an operation is of the utmosl importance. 
The patient should see and hear as little as possible of the operating 
room and of the preparations which are being made for the impend- 
ing operation. 

Struggling, and pressure upon the abdomen by gauze pud-, ban- 
dages, etc., may cause cardiac dilatation. The administration of 
morphin in moderate doses preceding the administration of ether 
is often advisable. It diminishes the amount of ether required, 
tends to prevent struggling, excitement, and acapnia, and in man 
does not impair vasomotor tone. Patients with heart disease, 
pneumonia, or empyema should be anesthetized gradually, in the 
sitting or semirecumbent posture (Gatch, Gann, and Maim. 1 

The Posture of the Patient. The posture of the patient during 
operations of necessity entails marked changes in blood-p] 
and blood distribution, with which the heart under the benumbing 
influence of anesthesia or if handicapped by disease, may be unable 
to cope. Thus in the morphinized animal carotid pressure falls 
owing to this effect of gravity in the head-up posture, and rises 
when the feet are uppermost. Compensation is established by 
cardiac and vasomotor reactions in the stronger animals, but 
rabbits die if the feet-down position is long maintained (fifteen 
minutes to two hours) from cerebral anemia, due to splanchnic 
dilatation which can no longer be overcome by respiratory move- 
ments (abdominal compression and diaphragmatic suction). The 
normal vasomotor tone is depressed by ether, and especially so by 
chloroform. Again, dogs may be killed by a prolonged Trendelen- 
burg position plus ether (not morphin) anesthesia, the death 
resulting from failure of respiration, the heart action remaining 
good and the blood-pressure high. While death may occur similarly 
in the horizontal position, partial or complete respiratory failure 
is more common in the head-down posture. 

1 The Danger and Prevention of Severe Cardiac Strain during Ether Anesthesia, 
Jour. Am. Med. Assn., 1913,. lx, 1273. 



404 BLOOD PRESSURE IN SURGERY AND OBSTETRICS 

Recenl researches indicate that "the Trendelenburg position is 
harmless for patients with normal hearts, provided that respiration 
is free an<l unobstructed." '1 liis "position should be used only 
with extreme emit ion in cases of cardiac disease." The position 
should Dot be established or relinquished suddenly. Using this 
posture forces a large amount of venous blood toward the heart, 
and, if this organ is capable of handling it, produces temporarily 
a marked increase of brachial blood-pressure. If the position is 
suddenly abandoned the venous pressure, and consequently the 
arterial pressure, fall and bulbar anemia may result, especially 
if vascular tone is depressed. 

The Effect of Chilling during Anesthesia. Under ether anesthesia, 
the application of cold to dogs produces a marked rise of blood- 
pressure; under chloroform no such rise occurs. It seems, therefore, 
that the narcotic dose of ether does not abolish vasomotor reflexes 
ns does chloroform. The rise of pressure in the former instance 
causes a congestion of the internal viscera, a condition comparable 
to what occurs during the act of "catching cold," and probably 
accounts for the greater frequency of respiratory infections after 
ether. 1 

Visceral Manipulation.: — Blood-pressure observations have taught 
the importance of avoiding, or at least minimizing, certain surgical 
manipulations. Thus a marked fall of pressure is caused by irrita- 
tion of the dura and of the subdiaphragmatic peritoneum, traction 
upon bloodvessels or nerves, renal or mesenteric vessels, the brachial 
plexus, or the testicles; by rough sponging, blunt dissection, exposure 
or rough handling of viscera, peritoneal flushing, separating adhe- 
sions, delivering tumors, extirpation of the kidney, exposure of the 
spinal cord, section of large nerve trunks unless previously cocainized. 
The upper portion of the peritoneal cavity is more sensitive than 
the lower. 

On the other hand, hlood-pressure rises during divulsion of the 
sphincter ani and in stretching of the sciatic nerve. 

The following procedures produce but slight blood-pressure 
changes: incision of the seal]), chiselling of bone, separation of 
the periosteum, hernia operations I without adhesions), the resection 
of ribs, appendectomy (simple), incision of the kidney. Dragging 
upon the mesentery produces a much greater fall of pressure than 
handling the omentum. Especial care should be exercised in the 

1 Stursberg: Das Verhalten d. Blutdrucks unter d. Einwirk. v. Tempera turroizen 
in Aether u. Chloroform Narkose., Mitt. a. d. Grenzgeb. d. Med. u. Chir., 1910, 

xxii, 1. 



MANIPULATION OF Till-: PELVIC VISCERA t05 

region of the duodenum, pylorus and gall-bladder, owing to the 
possibility of interfering with the circulation in the larger venous 
trunks. Trauma t<» the pelvic viscera, on the other band, has much 
less tendency to produce shock (Gatch). Under normal circum- 
stances the diaphragm materially aids the circulation by alternately 
increasing the pressure in the thoracic and in i be abdominal ca vil ies. 
Hut once the abdomen is opened, the diaphragm no longer increases 
intra-abdominal pressure during inspiration and hence less blood 
reaches the right heart. 

Concussion of the brain produces a fall of blood-pressure, com- 
pression, a rise (sec page 389), but severe experimental injury of the 
cerebral hemispheres under complete anesthesia does not cause 
a fall of pressure. "Collapse from interference with the medullary 
centres is of course not true surgical shock" (( !rile . 

Manipulations of the Thoracic Viscera. — The effects of various 
surgical manipulations upon the blood-pressure, pulse rate, and 
respiration have been made by Flint. 1 

The detailed results cannot be given here, but the conclusions 
reached show that "the reactions of the medullary centres to 
operative traumatism as shown in these experiments suggest that 
we should be cautious in the treatment of the parietal pleura, 
particularly in tearing it at the angles of the intercostal wound by 
injudicious application of the rib-spreader. The lungs may be 
handled freely, but manipulations that tend to transmit traction 
to the great vessels and bronchi at the root of the lung should be 
reduced to a minimum. In heart suture the Sauerbruch inn hod 
of temporary hemostasis leads to too serious a fall in blood-pressure 
to be safe except where other means of hemostasis fail. Any 
mechanical stimulation of the heart, either directly or through the 
pericardium, during suture, should be avoided so far as possible. 
Furthermore, in packing off the lungs to obtain an exposure of 
other thoracic viscera it would be wise to avoid any unnecessary 
trauma which might tend to reduce the blood-pressure excessively. 
These are the stimuli which, in the present set of experiments, 
have produced the most serious reactions." 

Manipulation of the Pelvic Viscera. — Manipulation of the pelvic 
organs during laparotomies may ^produce either a rise or a fall of 
pressure, depending upon the manner in which the viscera are 
handled. Experimental irritation of the genital mucous membrane 
(in dogs) produces a fall of pressure ranging between 5 and 50 

1 Flint, J. M.: Physiological Basis of Thoracic Surgery, Jour. Am. Med. Assn., 
1912, lix, 760. 



406 BLOOD PRESSURE IX SURGERY AND OBSTETRICS 

per cent. The fall of pressure is more marked if the stimulation 
is applied in the lower vagina; in the upper portion a rise of pressure 
may result. Irritation of the rectal mucosa causes a fall of pressure. 1 
Schroder found that manipulations of the female generative 
organs by way of the vagina caused less lowering of pressure than 
when a laparotomy was performed; but ( 'rile found that manipu- 
lation always produced a rise which was proportional to the 
traumatism. 

Aspiration of the Pleura.— Pleural effusions, if large in amount, 
tend to raise blood-pressure, unless sufficiently large to cause cardiac 
embarrassment. The increase in pressure, which is greater than in 
abdominal effusions, may amount to 20 mm. 

Vertigo, syncope, and even death may follow the withdrawal 
of fluid from the pleural cavity. It has been shown that these 
effects are not merely the result of altered pressure relations in the 
thorax, but that they are due to a depressor reflex originating in 
the pleura, which may be: (1) A central reflex cardio-inhibitory 
type, in which the heart is slow, intermittent, and there are great 
variations in the systolic and diastolic pressures, associated with 
slow respirations. (2) A vasomotor type showing a steady rapid 
decline of pressure without any great difference between the systolic 
and the diastolic readings. Respirations are shallow, sometimes 
rapid. This type, in contradistinction to the first, not infrequently 
terminates in death. The reflex may be either central or peripheral. 
To minimize the likelihood of these accidents care should be taken 
to avoid irritating the pleura with the trocar or drainage tube. 2 
In seven out of eight aspirations Clark found a fall of venous pressure 
(see page 230). 

Paracentesis Abdominalis.— This procedure is attended with 
much the same blood-pressure changes as those which occur when 
the pleura is aspirated. As might be expected a greater fall (32 nun. 
on the average) occurs. 

"Up to' a certain point the general arterial pressure increases 
with an increase in the pressure of intra-abdominal fluid; beyond 
this poinl the blood-pressure falls. Quirin attributes the early 
pise in blood-pressure to increased resistance by compression to 
the How of blood through the abdominal arteries; the fall occurs 
when the heart, handicapped by a diminished supply of venous 

i Belfield, W. .1.: Uebei depressonsche Reflexe, erzengl durch Schleimbautreifr; 
zung, Arch. f. Anat. u. Phys.. 1882, p. 198. „ JO tnm 

Blood-pressure Lowering Reflexes, Am. Jour. Mod. Sc, 1907, 
exxxh 



CATHETERIZATION OR DRAINAGE OF THE BLADDER L07 

blood, is qo longer able to overcome the resistance of the abdominal 
arteries. Ascitic fluids have an intra-abdominal pressure of 19 to 
li' nun. Hg.j according to Quincke. Quirin found that the intra- 
abdominal pressure fell H> to I I mm. after tapping, and that this 
corresponded with the simultaneous t';ill in arterial pressure of 5 
to 10 mm. Hg. after paracentesis in four cases. Cook ami Briggs 
record one case of abdominal paracentesis in which the pressure 
fell 35 mm. II»'. during the withdrawal." 1 

The rate of withdrawal is apparently more important than the 
amount so far as the immediate pressure is concerned. The ultimate 
pressure depends more upon the quantity of fluid withdrawn. 
External abdominal pressure favors a, rise of pressure, as does 

also tlie recumbent posture. "Improvement is mosl pronounced 
in those cases that undergo a marked fall in pressure during the 
operation" (Capps). 

The emotional disturbance entailed by a prospective operation, 
as well as the actual pain of puncture, produce a temporary eleva- 
tion of blood-pressure see under Abdominal Distention and Blood- 
pressure, page 268 1. 

The majority of surgeons seem to be impressed with the impor- 
tance of blood-pressure readings in bra n surgery. Horsley states 
that 2o per cent, of the sudden deaths after prolonged operation 
may be avoided by frequent observations. 

Catheteiization or Drainage of the Bladder. Drainage of the 
bladder, either by suprapubic incision or by a retained catheter as a 
preliminary procedure to prostatectomy, definitely lowers blond- 
pressure (average in 50 eases, 166 to 14.3 mm.) and diminishes 
mortality.- Peacock 3 says that in cases of chronic prostatic obstruc- 
tion, serious back pressure upon the renal circulation exists. 
Increased blood-pressure is a compensatory phenomenon necessary 
to maintain urinary secretion against back pressure. A sudden 
relief of vesical pressure, whether a result of catheterization or 
cystotomy, causes a prompt and marked fall of blood-pressure 
(20 to 100 mm.). This may result in anemia or uremia. To this 
"hidden nephritis," which occurs in from 25 to 50 per cent, of 
operative prostatectomies, rather than to shock or hemorrhage, 
he attributes the high mortality with which the operation is asso- 
ciated. He further suggests that the foregoing phenomena explain 

1 Capps, J. A. : Some Observations on the Effect on the Blood-pressure of the 
Withdrawal of Fluid from the Thorax and Abdomen, Jour. Am. Med. Assn., January 
5, 1907, xlviii. 

2 Balfour, D. C: Mayo Clinic, 1913, p. 73. 

3 Blood-pressure and Prostatectomy, Ann. Surg., 1916, lxiv, 659. 



\08 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

the advice aever to empty a distended bladder completely, since 
shock and even death may follow a simple catheterization. A pre- 
operative pressure much above 150 mm. markedly increases the 
risk entailed in cystotomy or prostatectomy. 

Anesthetics. Anesthetics differ in their effect upon blood- 
pressure, and the degree to which a given drug lowers pressure is 
an index of the danger with which its administration is associated. 

Ether. The early Stages of ether anesthesia are associated with 
an increased blood-pressure due to psychic stimuli and muscular 
effort. This increased pressure is maintained through stimulation 
of the respiratory centre. Recent experimental evidence has shown 
that ether alone, even when employed in large amounts, rarely 
produces much depression of blood-pressure. 1 When anesthesia 
is complete, the pulse rate and the blood-pressure are jiractkally 
normal. A slight postanesthetic rise is often observed, which the 
administration of oxygen generally increases. If the period of 
etherization exceeds one hour more or less peripheral vasodilatation 
occurs and tends to progress as time increases. As a general rule 
the maximum is not reached within seven hours; it may, however, 
appear much sooner.- During ether-oxygen anesthesia blood-pressure- 
is invariably increased. If ether is administered intravenously a 
preliminary rise of pressure (6 to 25 mm.) occurs to be followed at 
the end of from one to three hours by a fall of like degree (Honan 
and Hassler). A fall of pressure during anesthesia may result 
primarily from either vasomotor or from cardiac failure. Hender- 
son believes that both conditions are fundamentally due to acapnia 
resulting from excessive pulmonary ventilation in the stage of 
excitement. Prolonged ether-chloroform narcosis in rabbits is said 
to produce injury to the chromaffin system (Schur and Wiesel). 

The effect of morphin and ether anesthesia combined differs 
from that of ether alone. In the latter instance sensory stimuli 
are not completely blocked, although the sensorium is abolished and 
surgical anesthesia may be sufficient. 

Chloroform. Blood-pressure is often reduced even in the earlier 
stages (15 minutes); under full anesthesia a marked jail is often 
presenl which in fatal cases continues progressively until death 
occurs, due to cardiac depression. Even in the curlier stages, how- 

l Guy, W., Goodall, V., Eteid, II. S.: Blood-Pressure in Anesthesia, Edinburgh 
Med. Jour., L91 1, a. s., iii, 126. 

1 Mmis W. E.: Blood-pressure and Graphic Vasomotor Changes in the Per- 
iphery iliirint.' Ether Anesthesia, Ann. Surg., 1916, lxiv, 646. 

Primarj Eeaii Failure in Normal Subjects under Ether, Surg., ( lynec. ami I >bst., 
191 1, p. mi. 



ANESTHETICS 409 

ever, the heart may temporarily cease contracting, owing apparent l.\ 
to reflex inhibitory stimuli originating in the air passages. In ca e 
of a diseased heart the arrest may be permanent. The depressant 
action of chloroform upon the heart is much greater than thai of 
ether. Regarding the primary vascular effect of chloroform there 
is still divergence of opinion. Some investigations show an initial 
rise of pressure due to stimulation of the vasomotor centre. This 
stimulation docs not increase blood-pressure, as it i^ more than 
counter-balanced by cardiac weakness (Cushny). Unlike ether, 
chloroform docs not have any compensatory stimulating action 
to mask the effects of peripheral stimulation; it is this property 
which constitutes its danger ('<. Miiller). 11' oxygen is combined 
with chloroform blood-pressure is much less reduced than by 
chloroform alone. 

Ethyl Chloride. The effect of ethyl chlorideupon the heart muscle, 
similarly to that of chloroform, is depressive, but nineteen limes 
more of the former is required to produce similar results. Ethyl 
chloride causes local peripheral dilatation. Vagus inhibition of the 
heart occurs readily. In concentration of from L0 to 20 per cent, 
a fall of blood-pressure results from vagus stimulation. If 30 per 
cent, or more is used, blood-pressure falls from cardiac muscular 
depression, although this is not so pronounced as after chloroform. 
Ethyl chloride generally .-lows the pulse and produce-- a fall of 
blood-pressure. 2 It is by many regarded as a dangerous anesthetic. 
far inferior to nitrous oxide. 

Nitrous Oxide.- The administration of this drug i- attended with 
a slowing of the pulse and a marked rise of art, rial pressure. These 
effects have been attributed both to a specific action and to the 
asphyxia] condition of the blood. In arteriosclerosis, especially if 
associated with hypertension, it may cause vascular rupture, ('rile 
states that "under approximately equal trauma the changes in 
the brain cells were approximately three times as great under 
ether anesthesia as under nitrous oxide anesthesia; that the fall 
in the blood-pressure was on the average two and a half times 
greater under ether than under nitrous oxide; and finally, that the 
condition of the animal was better after trauma under nitrous 
oxide than after equal trauma under ether." 

When nitrous oxide oxygen is used, the primary rise is followed by 
a fall to normal which can be maintained by proper control almost 

1 Embley: Proc. Royal Soc, 1906; Lancet, April 20, 1907; Pharm. Jour., xxiv, 650. 

2 McCardie: The Position of and Mortality from Ethyl Chloride as a General 
Anesthetic, British Med. Jour., March 17, 1906, p. 616. 



410 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

indefinitely. A Midden increase of oxygen or cessation of the 
anesthetic causes a marked rise lasting fnmi five to fifteen minutes 
after the return to consciousness (Faught); 

Bloodgood 1 states that the average initial rise ranges between 
5 and 15 mm. Even in cases of arterial hypertension this anesthetic 
is considered safe. 

Morphin and Hyoscin. --These drugs are frequently employed 
hypodermically before the administration of nitrons oxid-oxygen 
anesthesia. The general result according to McKesson-' is a lowering 
of pressure o to 1") mm.— below the patient's normal; especially 
is this noticeable in hypertensive cases. 

Cocain. Cocain stimulates the heart muscle directly or as the 
result of accelerator influence 1 . In the early stages of intoxication 
there is peripheral vasoconstriction (local action and central stimu- 
lation) causing a rise of blood-pressure. Later, pressure falls 
owing to peripheral action. Cocain has been almost entirely 
supplanted by the less toxic drugs, stovain and novocain, the former 
being used for spinal and the latter for local anesthesia. 

The subject of anesthesia cannot, of course, receive prolonged 
consideration here, but a jew 'points may be emphasized. There 
seems to be no valid reason for chloroform as a substitute for ether 
in major operations. It should never be administered after a 
preceding period of ether excitement. For minor operations nitrous 
oxide is preferable. In using ether the subject should be quickly 
narcotized and kept "well under." Struggling during the adminis- 
tration and incomplete anesthesia are dangerous. The beneficial 
effects of rebreathing (CO2 stimulation) in preventing shock, as 
shown by Catch, lend strong support to Henderson's explanation 
of this condition as resulting from acapnia. The preliminary 
administration of morphin is often desirable. Nitrous oxide with 
oxygen is for short operations an excellent anesthetic. 

The Cerebrospinal Fluid and Blood-pressure.— The normal 
pressure of the cerebrospinal fluid ranges between 60 and 100 mm. 
I [ 2 ( ). It may be increased to 200 to 800 mm. in meningitis or brain 
tumor. It should never be reduced below 60 mm. II2O. It varies 
and is practically identical with the pressure in the venous sinuses. 8 
A relatively small increase in' cerebrospinal pressure stimulates 

1 Traumatic Shock and the Employment of Blood-pressure Estimations in Its 
Prevention and Treatment, Internal. .Imir. Surg., 1913, \\\i, 'MY.i. 
■ Blood-pressure under Anesthesia, American Year Book of Anesthesia and Anal- 
L915, i, 87. 
Itazi.T and Peet: Factors <>f Influence in the origin and Circulation of the 
< erebrospinal Fluid, Am. Jour. Physiol., 1914, p. nils. 



CEREBROSPINAL FLUID \.ND BLOOD-PRESSURE 411 

the vasomotor, cardio-inhibitory and respiratory centres. When 
pressure is increased considerably above the norma] arterial pressure, 
respiration ceases, and there is an enormous rise of arterial pressure 
with a slo\n pulse. When the cardio-inhibitorj centre becomes 

exhausted, blood-pressure rises still higher owing to the continued 

activity of the vasomotor centre, until the latter becomes par- 
alyzed, 1 whereupon blood-pressure falls. 

Lumbar Puncture. Blood-pressure is the mosl valuable guide 
during this procedure. A well-marked fall of tension indicates 
immediate cessation. Lumbar puncture is sometimes followed by 
sudden syncope especially when medicinal substances are injected. 
This may result from (1) the puncture of the dura a rare hut 
possible reflex disturbance; (2) increased intraspinal pressure; (3) 
the introduction of chemicals used tor purposes <>l' medication or 
for the preservation of sera. Auer's researches indicate thai tri- 
cresol, which is used for the last-named purpose, causes a greater 
fall of blood-pressure than chloroform or formalin. 

" 1. Tlu- puncture of the skin is accompanied by a rise in blood- 
pressure which varies in extent with the degree of consciousness, 
the pain, and the disturbance produced by the operation, hut which 
is not accounted for entirely by these factors. Puncture of the 
dura, causes a much larger rise, which is due not to pain or the 
disturbance produced hut to a definite effect on the vasomotor 
centre. Similar rises occur in dogs under full anesthesia. 

"2. Withdrawal of cerebrospinal fluid per se tends to lower the 
blood-pressure, but the net result of lumbar puncture is to raise i1 
for at least twenty minutes afterward. 

"3. The type of blood-pressure chart obtained in lumbar punc- 
ture, when the increased intracranial pressure is of subtentorial 
origin, is the same as that obtained in normal individuals; or 
as that obtained when the increased pressure is of supratentorial 
origin; but in the subtentorial types the variations are less pro- 
nounced. In subtentorial cases the rise is more sustained." 2 Blood- 
pressure readings should always be made during intraspinous 
medication. Berghausen 3 suggests that the needle be left in situ 
until blood-pressure returns to the same height as that at which it 
was preceding the spinal puncture. This seems hardly necessary 
if the serum has been given by the gravity method. According to 

1 Dixon and Halliburton: The Cerebrospinal Fluid, Jour. Physiol., 1914, xlviii, 317. 

2 Gray, H. T., and Parsons, L. : Blood-pressure Variations Associated with Lumbar 
Puncture and the Induction of Spinal Anesthesia, Quart. Jour. Med., 1911-12, v, 339. 

3 Intraspinous Medication, New York Med. Jour., 1914, c, 1006. 



412 BLOOD-PRESSURE /.V SURGERY AX J) OBSTETRICS 

the last-named author sudden respiratory changes follow only 
when blood-pressure change has been marked— usually after a 
fall of pressure (see Meningitis). If collapse symptoms occur, the 
head should be lowered, the feet elevated, and ether and strychnin 
should be given hypodermically. 

Spinal Anesthesia. " 1 . Blood-pressure records from eases of 
high spinal anesthesia show at the outset an abnormally high 
blood-pressure due to mental anxiety; then a rise following lumbar 
puncture; next a 'preliminary fall,' followed by a further more 
marked 'main fall' as the paralysis affects the thorax. Finally, as 
the paralysis passes off, the blood-pressure rises to its original 
values. The ' preliminary fall' is due to: 

" '/ 1 Flaccid paralysis of the abdominal and skeletal muscles. 
" (6) Subsidence of the disturbance caused by lumbar puncture. 
"(c) Onset of mental calm, amounting possibly to sleep. 

"The 'main fall' is due to the thoracic paralysis, which is not 
compensated for by overaction of the diaphragm, and consequently 
the aspiratory action of the thorax is diminished. 

"2. Marked deviations from this common type of chart are 
due to: 

" (a) Voluntary inspirations by the accessory respiratory muscles, 
and 

" (6) To a lesser extent by the activity of the higher centres. 

"Variations in the pulse rate do not. closely follow those of the 
blood-pressure, but a certain degree of resemblance is often seen 
owing to the consciousness of the patient. 

" :;. Vomiting during spinal anesthesia is due to thoracic paralysis, 
which induces either: 

"(a) Anemia of the medulla. 

"(b) Excessive action of the diaphragm, which interferes with 
the stomach. 

"4. Blood-pressure records from cases of low spinal anesthesia 
show the ' preliminary fall' but not the ' main fall." The ' preliminary 
fall' in these cases is due to: 

" in) Subsidence of the disturbance caused by lumbar puncture. 

" (\>) Onset of mental calm. 

" (c) In some cases from the degree of flaccidity of the abdominal 
muscles. 

" o. In the supine position there is no stagnation of blood in the 
great vessels, even when a very high spinal anesthesia is induced." 

Inasmuch as the normal blood-pressure depends upon afferent 
and efferent pressor and depressor stimuli it is evident that serious 



SPINAL I VESTHESIA 



413 



results may follow the cutting off of such impulses. A ce ation 
of pressor impulses, for instance, would leave the effect of depres jor 
fibers in predominance. 

The question of blood-pressure In spinal anesthesia is a complex 
one, owing to the physiological action of the substances employed. 
In fifty eases studied by Mori the results were verj variable owing, 
it seemed, to the inconstant effects of cocain, epinephrin, and the 
patient's psychic state. 1 George Miiller, in Frazier's Clinic at the 
University of Pennsylvania, found that lumbar puncture caused 
a marked elevation of the blood-pressure not due to the pain, 
because it occurs even under anesthesia. In corred spinal anesthesia 
the complete block of peripheral impulses makes the pressure curve 
independent of the nature of the operation. If the anesthesia is 



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Fig. 103. — Curve of relative amount of rise or fall in blood-pressure at end of 
operation: readings to left of zero, lowered after operation; to right, raised. (After 
Stanley.) 

allowed to extend upward it cuts off the pressor stimuli to the 
splanchnic area and may produce the effect of shock, or if it extends 
still farther upward, respiratory embarrassment or even paralysis 
may occur (see page 343). Smith 2 states that blood-pressure can 
be as profoundly lowered by spinal anesthesia as by section of the 
cervical cord. The greatest fall occurs when injections are made 
in the thoracic region, at which point the splanchnic vasomotor 
fibers are given off. This part of the vasomotor mechanism is 
first affected when injections are made in the lumbar region. It 



1 Mori, M. : Das Verhalten des Blutdruckes bei Lumbalanasthesie, Deutsch. 
Ztschr. f. Chir., 1904, lxxiv, 173. 

2 Blood-pressure in Spinal Anesthesia, Boston Med. and Surg. Jour., 1915, exxiii, 
502. 



414 BLOOD PRESSURE IN SURGERY AND OBSTETRICS 

appears that diffusion of the drug depends greatly upon the bulk 
of the injection the more fluid injected, the greater the diffusion. 
The most pronounced effects on blood-pressure occur when epi- 
aephrin was used in conjunction with novocain. Efforts to raise 
the fallen pressure by the intravenous infusion of epinephrin and 
pituitrin result in only a transient rise. 

In a studj of l'si) cases Stanley 1 found that blood-pressmv was 
more frequently lowered than raised by spinal anesthesia produced 
by tropacocain hydrochloride. This is shown by the chart en page 
113, from which it will he noted that the greatest fall of blood- 
pressure amounted to 88 mm. Hg., whereas the maximum rise was 
equivalent to 38 mm. Hg. Despite the fall of pressure the patients' 
general condition did not require treatment therefor. 

Hemostasis by Belt Constriction. (Momburg). — As a means of 
checking hemorrhage after severe trauma, in obstetrics, etc., with 
certainty, without an assistant and without the danger of local 
wound infection, Momburg has sugggested winding a rubber tube 
tightly around the waist, one turn after another, until the femoral 
pulse disappears. This procedure, which causes a sudden rise of 
blood-pressure and which throws a corresponding burden upon the 
heart, should- not be employed in case of cardiovascular disease. 2 
The suddeniK ss of the cardiac strain may be somewhat mitigated 
by preliminary constriction of the thighs. It is absolutely essential 
that the constriction be very gradually relieved so that vasomotor 
tone and the distribution of blood may be gradually reestablished. 
It should never be applied in the case of elderly or obese women. 
Numerous accidents have occurred from defective technic. This 
procedure has not met with any practical acceptance, and is by 
many authorities condemned as a, dangerous and unjustifiable 
procedure. 

Abdominal Conditions. — Blood-pressure readings may be of diag- 
nostic value in abdominal lesions. Thus unilateral suppurative 
renal disease causes a rise of pressure which falls after evacuation 
oi- extirpation. 3 Headings are of value in the diagnosis in visceral 
rupture, ectopic pregnancy, gastric or intestinal perforation, etc., 
all of which conditions cause a sudden and often marked fall of 
pressure. As a rule the extent of the fall depends upon the patient, 
the size of the perforation, the coexistence of hemorrhage, the 

'Spin;,] Anesthesia, Jour. Am. Med. Assn., L916, brvi, L090. 
2 For detailed study sec Adair, I". I>. : Surg., Gyneo. and Obst., 1912, p. 112. 
Iviim and Kotzenberg: (Jeber d. Verhalten d. arteriellen Blutdruckes bei chirur- 
gischen Nierenerkrankungen u. Appendicitis, Beitr. /,. klin. C'liir., l'.tus, Kiii, KM. 



ABDOMINAL CONDITIONS 115 

presence of localizing adhesions, and the portion of the peritoneum 
involved. The larger the perforation, the less ii is walled off; 
the greater the associated hemorrhage and the higher its location, 
the more will arterial pressure fall. The pain which often precedes 
or is associated with perforation causes a preliminary rise of press ure. 
Pressure readings naturally have a much greater value if the 
patient's normal pressure is known. Hence the value of routine 
pressure records. It is impossible to give any rules based upon 
absolute figures, but a systolic pressure below 90 mm. Hg. in asso- 
ciation with other signs would point to hemorrhage or perforation 
even in toxic patients prostrated l»\ typhoid fever (see page 215). 
Acute inflammatory lesions in the peritoneum, such as appendicitis 
in the early stages, may cause a slight increase in blood-pressure, 
whereas renal colic, plumbic cramps, and tabetic crisis generally 
show a marked rise in tension. The onset of peritonitis is accom- 
panied by a distinct increase of pressure which gradually falls 
with increasing toxemia. The rise is due to local pressor, the fall 
to central depressor, impulses. 

The Application of Heat and Cold. Heat applied to the external 
abdominal wall produces a rise of blood-pressure, whereas cold has 
but little if any, such effect. But applied within the peritoneal 
cavity, both heat and cold produce a marked tall of pressure. This 
is probably due to stimulation of the splanchnic nerve. 1 The em- 
ployment of hot cloths or saline solution in abdominal operations 
ma\ therefore have deleterious effects. 2 

The custom now instituted in all up-to-date clinics of having the 
anesthetist or his assistant chart the pulse rate and blood-pressure 
during the course of anesthesia, with the addition of occasional 
notes dictated by the operator, is most commendable. It is not 
only a signal assistance to the surgeon at the time of the operation, 
but it also leads to a more careful analysis of the effects of anesthesia 
and trauma, and furnishes permanent records for statistical stud}\ 

Practical Considerations in Regard to Shock. — Blood-pressure should 
be estimated before, rather than on, the day of the operation. 
Certainly it should be taken in the ward and not in the anesthetiz- 
ing room, otherwise fallaciously high readings will be obtained 
(10 to 20 mm.). 

Shock is a condition of gradual, not sudden development. It 
cannot be detected by palpating or counting the pulse since a large 

1 Burton-Opitz: Am. Jour. Physiol., 1916, xli, 103. 

2 Hanimett, F. S., Tice, E. W 7 ., and Larson, E.: Blood-pressure Changes Induced 
by Hot and Cold Applications on and within the Abdomen, Jour. Am. Med. Assn., 
1917, lxviii, 621. 



416 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

pulse-pressure may yield the impression of a "good pulse" even 
when a falling diastolic pressure is already dangerously low; further- 
more, the pulse rate is not always rapid. Shock is to be feared, 
however, it' with an increasing pulse rate pressure remains stationary, 

or what is worse, actually decreases. Without a fall of pressure no 



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Fig. 104. — Chart from a case of gastromesenterie ileus, together with pyloric 
stenosis due to a bealed ulcer, requiring a pyloroplasty in addition to resection of the 
righl half Of the colon. The operation lasted three hours and twenty minutes. No 
i-ihei u;is used. A marked fall of pressure occurred while closing the peritoneum. 
This was remedied by temporarily placing the patient in the Trendelenburg position. 

Sudden cyanosis With a second fall of pressure occurred while the abdominal wound 
was being closed. The nitrous oxide was stopped and the operation finished under 
Local anesthesia. Salt solution, strophanthin, and the inverted posture again 
restored the patienl to a satisfactory condition. (After Bloodgood.) 



serious shock can occur. Variations of in to 15 mm. are not a cause 
for apprehension but a continuous fall with a rising pulse rate is an 
urgent indication for treatment. Fall of pressure may begin from 
five i" twenty minutes after the exciting cause, such as rough 
handling of the viscera, traction on the mesentery, extensive walling 



MENSTRUATIOh 117 

off of the viscera with gauze packs, hemorrhage, excessive adminis- 
tration of the anesthetic, etc. The sequence of events is usually 
a fall of diastolic pressure, increased pule rate, decrease of pulse- 
pressure, until eventually with a diastolic pressure of 60 the pulse- 
pressure is only 20 and the pulse raic over 120. This picture 
represents a typical severe case of shock, to which if it lasts half an 
hour the patient usually succumbs, although life may be prolonged 
for two or three days (McKesson) . 

Shock as a. cause of death stands relatively high in operations 
immediately after accidental injuries, in acute and chronic infectious 
disease, cachexia, inanition, and in toxemia such as exophthalmic 
goitre, auto-intoxication from intestinal obstruction, trypsin poison- 
ing in acute pancreatitis, uremia, diabetic coma and obstructive 
jaundice I Bloodgood). 

Menstruation.— Blood-pre>-iu-e frequently rises for a day or 
two preceding the onset of menstruation. There is a fall of blood- 
pressure during the period which occurs independently of the loss 
of blood, and which lias been attributed to a slowing of the pulse 
and to psychic factors. 1 It is lowest on the second day of the How 
and is not much affected by the occurrence of pain at this time. 2 
Large doses of atropin (0.0007.1 gm. hypodermically) have some- 
times been successfully used in the treatment of dysmenorrhea of 
the spasmodic type associated with cramp-like pain a day or two 
before the onset of flow, especially in vagotonic cases. Much stress 
has been laid by Stolper upon the importance of blood-pressure 
estimations in the proper selection of cases. He states that women 
with a normal or slightly increased pressure during the inter- 
menstrual interval react most promptly to atropin, whereas those 
with a marked increase in blood-pressure show less response. 
Bogdanovics 3 and others have reported a premenstrual rise of blood- 
pressure in normal women, followed by a gradual decline after the 
onset of flow. Based upon pulse rate, blood-pressure, temperature, 
and muscular strength tests, the statement has been made that a 
cyclic rhythm occurs in normal women which renders them subject 
to periodic intervals of inefficiency. 4 The recent studies of King 5 

1 Wiessner, M.: Ueber das Verhalten des Blutdruckes wahrend der Menstruation, 
etc., Leipsic, 1904. 

2 Tenji, T.: Ueber d. Verhalten des Blutdruckes zw. d. Menstruellen u. nicht 
Menstiuelien Ztschr., Arch. f. Gynak., 1909, lxxxix, 517. 

3 Zentralbl. f. Gynak., 1910, xxxiv, 994. 

4 Jacobi: The Question of Rest for Women during Menstruation, Boylston Prize 
Essay, 1876. 

5 Concerning the Periodic Cardiovascular and Temperature Variations in Women, 
Am. Jour. Physiol., 1914, xxxiv, 203. 

27 



418 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

indicate that this tendency has been overemphasized and insofar 
as observations are concerned, made upon the systolic, diastolic 
and pulse-pressures of eleven women, such irregular results were 
obtained that they do not support the wave theory. Balard and 
Sidaine 1 were unable to establish any constant relationship between 
pulse rate, blood-pressure and menstruation either in different 
women or even in the same women at different periods. 

The Menopause. — Circulatory abnormalities are of frequent 
occurrence during the menopause. Among these "flashes of heat," 
formication, numbness, vertigo, cardiac palpitation, dyspnea on 
exertion, etc., may be encountered. A rise of arterial pressure is 
not uncommon after the cessation of menstruation. Whether it is 
merely a symptom or, as Potter- suggests, the cause of the symptoms, 
is uncertain. The diastolic does not increase proportionately with 
the systolic pressure. Pulse-pressure is thus increased. Further- 
more, the increased pressure is an irregular and intermittent one. 
In some cases hypotension with systolic-diastolic deviation occurs. 
Culbertson 3 states that the administration of extract of corpus 
luteum brings about a gradual restoration of blood-pressure to- 
gether with the disappearance of mental symptoms. If pressure 
changes are marked and prolonged the possibility of renal disease 
must be borne in mind. Engelhorn 4 has reported a marked allevia- 
tion of symptoms such as "hot flashes" as a result of phlebotomy. 

Ovarian extirpation clinically often produces evidences of increased 
irritability of the sympathetic nervous system. This has been 
substantiated experimentally, since this operation in bitches results 
in from six to eight weeks in a markedly increased vasomotor 
reaction after one injection of nicotin. The reaction to epinephrin, 
however, is not increased. 5 Jaschke 6 considers increased blood- 
pressure the most pronounced result of cessation of ovarian secre- 
tion and explains its absence when not present as a result of vicarious 
function of other endocrine glands. But Dubois and Waltham did 
not corroborate Jaschke's findings. They failed to get either hyper- 
tension or adrenalin glycosuria when the climacteric had been 
artificially induced. 

1 Arch. Mens. d'Obstet., January-March, 1916, v. 

2 Blood-pressure at the Climacteric, British Med. Jour., December 2, 1911, p. 1472. 

Study of the Menopause with Special Reference to Vasomotor Disturbances, 
Surg., Gynec. and Obst., 1916, xxiii, 667. 

: Munchen. med, Wchnschr., 1915, lxii, No. 45. 

6 Hoskins and Wheelon: Ovarian Extirpation and Vasomotor Irritability, Am. 
Jour. Physiol, 1914, xxxv, 119. 

6 MuiK-hon. incil. Wchnschr., November 9, 1915. 



PREGNANCY 419 

Extirpation of the testes is followed by a fall of blood-pressure, 
and the reaction to nicotin is constantly lowered. 1 The pn ence of 
successful testicular grafts iii any portion of the bodj reestablishes 
the normal vasomotor response. 2 It would seem, therefore, that 
normally functionating testes bear a relationship to irritability of 
the sympathetic. 

Pregnancy.— Systolic blood-pressure ranges between 100 and L30 
in about 80 per cent, of pregnant women. In about L0 per cent. 
pressure will be found below LOO mm. It has been stated 3 thai 
cases with pressures of less than 90 nun. are apt to exhibit signs of 
shock at the time of delivery, but [rving 4 did not corroborate this. 
The remaining L0 per cent, of cases will show a pressure of 130 or 
more. 

The importance of blood-pressure observations in pregnancy is 
universally recognized since hypertension is a more important and 
reliable index of toxemia than is albuminuria. This statement applies 
both qualitatively and quantitatively. Subsidence of the uterus 
may be associated with a slight fall in pressure. The normal rela- 
tions between systolic and diastolic pressure should remain constanl . 
Cases showing a pulse-pressure of or over 50 mm. should be watched 
and are benefited by digitalis."' Edema in pregnancy bears no 
constant relation to blood-pressure. 6 

What was previously described as the normal cardiac hyper- 
trophy in pregnancy is really only a change in the lateral percussion 
area, due to the more transverse position of the heart which the 
upward pressure upon the diaphragm entails (Stengel and Stanton). 
This transverse position tends to cause a kinking of the large 
vessels, which adds to the work expended by the heart, and in the 
case of a diseased myocardium this factor may become important. 
It also explains the occurrence of accidental pulmonary murmurs. 

The normal blood-pressure during the second stage of labor, if 
taken between uterine contractions, ranges between 130 and 150 
mm. After delivery normal values are reestablished. This fall 
is due to fatigue, cessation of excitement, and pain, as well as to 

1 Wheelon, H.: Influence of Testes on Blood-pressure, Am. Jour. Physiol., 1914, 

XXXV. 

2 Wheelon, Homer and Shipley: The Effects of Testicular Transplants upon 
Vasomotor Irritability, Am. Jour. Physiol., 1916, xxxix, 394. 

3 Lynch: Sxirg., Gynec. and Obst., 1913, xvii, 472. 

4 The Systolic Blood-pressure in Pregnancy, Jour. Am. Med. Assn., 1916, lxvi, 935. 
(An excellent article based upon a study of 5000 cases to which I am indebted for 
much information.) 

5 Hirst, J. C: Blood-pressure in Pregnancy, Penn. Med. Jour., May, 1915, p. 615. 

6 Rosensohn, M. : Parallel Study of Blood-pressure, Urine and Edema in Preg- 
nancy, Bull. Lying-in Charity, City of New York, January, 1917. 



120 BLOOD PRESSURE IX SURGERY AND OBSTETRICS 

vascular relaxation in the splanchnic domain. During the pains 
pressure estimations cannot well be made, but doubtless the pain 
as well as the abdominal compression cause much higher blood- 
pressure. Rupture of the membranes usually produces a marked but 
temporary fall in pressure. The birth of the child is again followed 
for a time by a fall of from 60 to 90 mm. 1 These changes in blood- 
pressure are due to the sudden diminution of intra-abdominal 
Tension, to which it takes some time for the vasomotor system to 
accommodate itself. Large hemorrhages tend to delay the return 
of pressure to the normal. 

Elevated Blood-pressure, Albumini hi \ and Toxemia According 
to Age. (Irvinc) 

^_ _ Percentage of , 

Number of Elevated 

Age. Mi '(>i]-pressure. Albuminuria. Toxemia. 

I H.l.r 20 421 11.4 20.0 2.8 

20 to 30 3165 8.9 13.7 1.0 

30 to 40 1283 14.3 12.2 1,5 

Over 40 131 22.1 17.5 1.5 

Although increased pressure is more common in elderly gravidas, 
it is in such cases less important as an evidence of toxemia than 
in younger women. Hypertension unaccompanied by albuminuria 
or other evidences of toxemia is not unusual and often responds 
to free purging. "A progressively rising blood-pressure, often 
from a low level, even though it never reaches the arbitrary danger 
point, should be regarded with apprehension as a most valuable 
sign of approaching toxemia" (Irving). 

It is of course important to know what a woman's normal pressure 
range is before drawing conclusions, but as a general rule eclampsia 
does not occur with a pressure below 150. When eclampsia does 
occur, pressures in the neighborhood of 200 mm. are usual ami 
generally associated with albuminuria. 

Elevated Blood pressure, Albuminuria and Toxemia According 
to Parity. (Irving.) 

, Percentage of , 

Number of Elevated 

Parity. cases. blood-pressure. Albuminuria. Toxemia. 

Primparaa 1679 12.2 14.8 1.1 

Secundiparas .... 1036 7.5 11.7 0.8 

Tertiparas 696 7.9 11.8 1.0 

Quartiparas .... 508 11.8 14.6 1.4 

Quintiparas .... 360 8.9 10.6 0.6 

Sextiparaa 261 10.7 9.2 0.8 

Beptiparae 177 13.8 11.4 0.6 

Beynemann, 'Hi.: Herz u, Zwerchfellstand wahrend Schwangerschaft, Ztschr. f. 
Cieburt.sli. u. Gynak., 1913, Ixxiv, 854. 



VRE I / VENT OF ECLAMPSIA 421 

.1 rising pressure (luring the latter part of pregnancy is the most 
const, int symptom of gestational toxemia and is a frequent pre- 
cursor of eclampsia (Hirst). 1 The hypertension increases with the 

severity of the attack. Many of Edgar's cases showed pressure- of 

200 mm. or more. "A fall of blood-pressure with amelioration of 
the other symptoms is the most favorable prognostic sign, bu1 
with aggravation of other symptoms indicates impending death." 

Intermissions with lowered pressure are favorable omens. The 
other symptoms are generally an increased pulse rate, epigastric 
pain, headache, visual disturbances, edema, albuminuria. ( 
with renal disease rarely pass through the period of gestation 
without some manifestations of toxemia. The absence of increased 
blood-pressure does not always exclude the possibility of eclampsia; 
the presence of high pressure between convulsions does exclude 
epilepsy (Chirie) . 

In the early stages of toxemia, gastro-intestinal symptoms may 
be marked before blood-pressure changes are obvious, and fatal 
convulsions may not be attended by a pressure over 160 mm. 
Hirst has reported a reading of 320 mm. in eclampsia and 192 mm. 
in a case of toxemia without eclampsia. He has seen recovery in 
two cases with pressures of 420 and 400 mm. respectively, showing 
that the danger of death is not necessarily proportionate to the 
height of pressure. The average eclampsia pressure ranges between 
190 and 200 mm. 

The administration of ergot does not appear to raise blood- 
pressure in the toxemia of pregnancy (see page 344), but the employ- 
ment of pituitrin may cause a very marked rise (Hirst). 

Summary. — During pregnancy a pressure of 125 mm. is normal; 
a pressure between 125 and 150 is to be regarded with suspicion; 
while a pressure of over 150 if accompanied by other toxemic 
symptoms calls for prompt and energetic treatment; often the 
induction of premature labor (J. C. Hirst). 

The Treatment of Eclampsia. — Some obstetricians of wide ex- 
perience recommended the use of veratrum viride in the treatment 
of eclampsia. Hirst states that "the most successful remedial 
measures are those which reduce blood-pressure most quickly and 
most effectually, such as puncture of the membranes, sweating, 
purgation, venesection, veratrum viride, and nitroglycerin," while 
Edgar writes: "I prefer ether, veratrum viride, glonoin, and chloral 
in the order named." Now clinical results are of primary impor- 

1 The Importance of Blood-pressure in the Toxemia of the Latter Half of Preg- 
nancy, New York Med. Jour., 1910, xci, 1204. 



422 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

tance, but in view of some definitely established faets it would 
appear that they are open to revision. We have seen under the 
discussion of nephritis that hypertension often appears to be 
Nature's defense against anuria and coma, and the most experi- 
enced clinicians no longer attempt to reduce blood-pressure by 
direct means except in eases of an emergency. Is eclampsia such 
an emergency? The reduction of pressure allays the convulsions, 
but is this due to the fact that the patient is too depressed to 
respond to stimuli? It has been established that collapse and 
shock are associated with and are in part the result of low blood- 
pressure. By administering cardiovascular depressants are we 
not reducing our eclamptic patient to a condition of collapse? It 
lias been shown that rapid emptying of the uterus in eclampsia 
frequently produces a fall of blood-pressure amounting to 100 mm. 
Hg., while a full dose of veratrum viride of itself may cause a 
depression of 145 mm. 1 It is unpleasant to contemplate the degree 
of blood-pressure fall which a combination of these two procedures 
might entail. Even if the eclamptic rise of pressure is not of a 
protective nature, and even if it should appear desirable to lower 
pressure by medicinal means it would seem far preferable to do 
so by the administration of the nitrites — drugs which do not also 
depress the heart and the medullary centres. Chloroform is 
undesirable not only because of its effect upon the heart, but also 
on account of its tendency to produce necrosis of the hepatic cells. 
Eclampsia is more than a vascular crisis, and while much higher 
blood-pressure favors and doubtless precipitates visceral hemor- 
rhages, such a rise of tension is only a symptom and not the basis 
of gestational intoxication. So far as the writer is aware, blood- 
pressure readings yield no clue as to the relative indication for 
immediate Cesarean section or conservative treatment. 

Hyperemesis gravidarum is usually associated with hypotension 
perhaps as a result of impoverished nutrition, 2 and indicating that 
the toxin is different from that causing eclampsia. 

In extra-uterine pregnancy the occurrence of anemia with a fall 
of pressure is the most important indication of internal hemorrhage 
(Homer). 

Attention has been called to the fact that shock associated with 
and probably due to low blood-pressure may, even in the absence 
of large hemorrhages, lead to sudden death during childbirth. 

1 Baile ock in Eclampsia, Am. Jour. Obst., 1911, lxiv, No. 2. 

• \\ allich, \ .: l/li\ pertenaon gravidique, Ann. d. Gynec. et d'Obst., 1912, xxxix, 
653. 



BLOOD PRESSURE OBSERVATIOh S Dl Ul \ <: ANESTHESIA 123 

Women with pressures not exceeding 90 mm. may pass through 
labor normally, but such low readings, especially if associated 
with anemia, always indicate special care and the institution of 
such measures as tend to prevent shock. 1 Poorly developed, 
neurasthenic women or women with contracted pelves often have 
low pressures. 

Fibromyomata of the Uterus. — There is no definite relationship 
between uterine fibromyomata and blood-pressure. In 148 cases 
studied 2 the height of the pressure seemed entirely independenl 
of the size or character of the tumors before operation. After 
operation 3 cases showed an unchanged pressure, 11 an increase 
of from 5 to 65 mm., and 8 a decrease of from ."> to 40 mm. Ilg. 





« • 


1 


f:-2r< 






1ft- ' mi 







Fig. 105. — McKesson's sphygmomanometer for use during operations. (Gwathmey.) 

Scopolamin-morphin. — The employment of scopolamin-morphin 
analgesia in labor has little or no effect upon blood-pressure. 
Baer's 3 cases showed an average drop of 5 mm. 

Blood-pressure Observations during Anesthesia. — With the 
intention of rendering blood-pressure readings much easier during 
anesthesia, Nicholson has fitted his new pocket sphygmoman- 
ometer with a Fedde indicator, in which a pith-ball plays up and 



1 Lynch, F. W.: Blood-pressure during Pregnancy, Surg., Gynec. and Obst., 
1913, xvii, 472. 

2 Taylof~and White: Blood-pressure in Fibromyomata Uteri, Surg., Gynec. and 
Obst., 1916, xxii, 216. 

3 Scopolamin-morphin Treatment of Labor, Jour. Am. Med. Assn., 1915. lxiv. 1723. 



424 BLOOD-PRESSURE IN SURGERY AND OBSTETRICS 

down as long as pulsations of pressure are transmitted to it. This 
is attached to the left-hand side of the box and connected up with 
the manometer and two cutis, one above and one below the elbow 
or knee-joints. 

An air-pressure of about 80 mm. may he maintained in the lower 
cuff throughout the operation, and the character, volume, and rate 
of the pulse noted continuously. The anesthetizer inflates the upper 
cuff with one hand whenever he desires to know the systolic pressure, 
simpK noting the height of the mercury column when the pith- 
hall ceases oscillating. lie then releases the air-pressure in the 
upper cuff and continues the anesthesia. In perineal operations 
the cuffs are placed on the arm and forearm instead of the thigh 
and leg. 



CHAPTER Will. 



OPHTHALMOLOGY. 



Since the ophthalmoscope is the only instrument which renders 
the naked arteries and wins visible during life it is not surprising 
that important data regarding blood-pressure or stasis, or vascular 
degeneration should be forthcoming from this source. The char- 
acteristic retinal lesions due to arteriosclerosis and arterial hyper- 
tension are not infrequently discovered by the ophthalmologist 
before other symptoms cause the patienl to consult his physician. 
Ophthalmoscopic examinations are of value t<> the student of 
blood-pressure no less than are sphygmomanometric estimations 
to the ophthalmologist. 




Fig. 106. — Rubino's modification of the Bloch-Verdin Sphygmometer. 



Blood-pressure in the Retinal Arteries.— The maximal pressure 
in healthy retinal arteries ranges between SO and 112 mm. Hg., 
according to Rubino, who has modified the Bloch-Yerdin apparatus 
for its measurement. The determination is based upon the principle 
that a certain pressure exerted upon the eyeball will arrest the 
circulation, this being indicated by the temporary loss of sight in 
the eye in question (Fig. 107). 

The Relation of Blood-pressure to Ocular Tension.— For practical 
purposes the eye may be regarded as an inelastic capsule, having a 
tension greater than the atmosphere, which varies as the intra- 
ocular contents are increased or decreased. Such changes are 
brought about mainly by alterations ' in the blood supply, the 
vitreous or the aqueous. "The circulatory conditions in the eye 



126 



OPHTHALMOLOGY 



resemble those in the intracranial cavity, with the exception that 
the infra-ocular is much higher than the intracranial pressure, 
and is therefore not affected by changes in the general venous 
pressure" Hill and Flack 1 ). Intra-ocular tension generally varies 




Fig. 107. — The Rubino instrument in use. 




Fie;. ION. — The Bajardi instrument for estimating retinal arterial pressure. 2 



with arterial pressure, but peripheral vasodilatation which lowers 
systemic pressure tends to increase intra-ocular pressure. Normally 
any change of tension is compensated by a reciprocal lymphatic 



1 I. The Relation between Capillary Pressure and Secretion. II. The Secretion 
of Aqueous and the Intra-ocular Pressure, Proc. Roy. Soc, Series B, August 12, 
L912, xxv. 

2 La Pressione del sangue nelT arteria retinica e suoi rapporti con la pressione nel 
n-i-n^d del Willis, Riforma Med., I'.Ul, xxvii, 1345. 



RELATION OF BLOOD-PRESSURE TO OCULAR TENSION 127 

flow. Excluding external causes (eyelids, ocular muscles, tumors of 
the eyeball or orbit), changes in tension mean loss of secretory 
compensation, which may come about "either by mechanically 
blocking the normal excretory channels or by so altering the normal 
ciliary secretion as to interfere with its ready interchange" — the 
"secretion" of the ciliarj body is not truly a secretion in the physi- 
ological sense of the term, bu1 an osmotic process, the pa 
fluid through a dialyzing membrane. There are no lymphatics 
in the eye, and the iris and vitreous have no secretorj function." 
According to Starling and l fenderson t he difference between arterial 
and intra-ocular tension averages 84 mm., and it is upon these 
pressure differences that the rate of secretion depends. The specific 
gravity of the secretion varies directly with blood-pressure and 
inversely with ocular tension. "Permanently increased tension 
is not due to high blood-pressure directly, hut may coexist with 
it only in the absence of adequate compensation" tbershoff) 
(see page L6). 

The foregoing statement- are generally accepted. In opposition 
to them Henderson believes that intra-ocular and intracranial 
tension run closely parallel. The latter depends much more upon 
the general venous than upon the general arterial pressure. It 
varies directly and absolutely with the pressure in the vena cava, 
which makes itself felt at once by backward pressure on the cerebral 
venous capillaries. A rise of arterial pressure only produce- a 
proportional rise in the intracranial pressure, because between 
the aorta and the cerebral veins lies the unknown and varying 
resistance of the arterioles. 

Based upon experimental evidence, Henderson believes that 
what has just been stated regarding intracranial tension applies 
to intra-ocular pressure, except that response in the latter is less 
prompt owing to the ramifications of the ocular veins. Therefore 
"the intra-ocular pressure must be the same as the intra-ocular venous 
pressure" Since the corneoscleral envelope is an unyielding case 
with a fixed cubic capacity, analogous in every respect to the bony 
cranium, the intra-ocular pressure is not a question of volume of 
the intra-ocular contents but purely a question of pressure of a 
fixed volume, which is governed in turn by the intra-ocular and 
general venous pressure. The intra-ocular pressure therefore 
represents "the pressure which remains in the eyeball after the 
force of the heart has been expended in driving the blood through 
the intra-ocular arterioles. On account of the elastic nature of the 
circulatory system of tubes a rise of arterial pressure can only 



128 



ol'/ITHALMOLOGY 



produce an increase in intra-ocnlar pressure in proportion as the 
resistance in the arterioles is overcome and intravenous pressure 
raised." 1 

The Estimation of Intra-ocular Tension.— The old method of 
gauging ocular tension, which for practical purposes may be con- 
sidered synonymous with intra-ocular pressure, by means of the 
fingers, is for obvious reasons falling into disuse when anything 
like accurate measurement is desired. The tactus eruditus cannot 
compete with instrumental precision. Sev- 
eral instruments are now available for the 
purpose. Among these the Schiotz tonometer 
has received widespread commendation (see 
Fig. 109). 

Intra-ocular tension is rated with this 
instrument by measuring the depth of the 
depression produced in the anesthetized 
cornea by the weight of the shaft of the 
tonometer; the higher the tension the less 
the depression. The data obtained are, 
however, based upon (1) the elasticity of 
the sclera and cornea, (2) the intra-ocular 
tension, and (3) the condition of the ocular 
drainage system. 2 Normal readings should 
not exceed 20 mm. Hg.; the normal pressure 
is about 20 mm. 

As with other ocular tonometers, consider- 
able practice is required before accurate 
readings can be obtained. Even with careful 
application considerable discomfort to the 
patient is entailed. No pressure should be 
made upon the eyeball except that exerted 
by the weights. 
The Stephenson tonometer is applied over the closed upper lid. 
It is furnished with a handle for holding it in position on the patient's 
face and with a milled head for adjustment to varying depths. 
The end of the inner tube, which consists of a concave cup, contains 
a spiral spring actuated by a jointed lever. The instrument is 
adjusted to zero, the lexer makes pressure upon the eye, and the 
moment at which indentation occurs is shown on the indicator. 




Fig. 109.— The Schiotz 
tonometer. 



1 Henderson, T.: Glaucoma, London, 1910. 
'Schdnberg, M. J.: Experimental Study of Intra-* 
Drainage, Jour. Am. Med. Assn., L913, Ixi, L098. 



ular Pressure and Ocular 



OCULAR LESIONS AND ARTERIAL PRESSURE 420 

Since the tension of the orbicularis palpebrarum and the recession 
of the eyeball into the orbit arc fairly constant in a given individual, 
temporal variations of pressure can be estimated. The technic 
with tins instrument is easily acquired. No anesthetic is necessary 
and readings maj be made in aboul one minute. Jus1 what pro- 
portion of the pressure obtained is true intra-ocular tension and 
how much is pressure of the retrobulbar tissues is as yet not posi- 
tively determined.' 

Ocular Lesions due to Increased Arterial Pressure. This subject 
cannot of course be discussed here in extenso. " In the later stages 
of intra-ocular vascular disease, hemorrhages frequently appeal. 
If centrally placed, their very position interferes with vision, or 
they may invade the vitreous, may result in proliferating retinitis, 
may cause glaucoma, and, if extensive, detachment of the retina. 
Closely allied to vascular changes arc also lenticular cataract, some 
varieties of optic atrophy, and some cases of retrobulbar neuritis" 
(de Schweinitz). According to William V. Norris, retinitis in some 
form occurs in not less than 25 per cent, of all cases of Bright's 
disease seen in general hospitals. 

In a study of 104 eases of ocular disease, Peter 2 found 1>I I- 

pressure as follows: 

9 syphilitic neuroretinitis, average systolic blood-pressure . . 132 mm. 
3 chronic parenchymatous nephritis, average systolic blood- 
pressure 132 " 

20 retinitis, average systolic blood-pressure 165 " 

59 neuroretinitis, average systolic blood-pressure .... 185 " 

3 albuminuric retinitis, average systolic blood-pressure . . 1!hi " 

6 hemorrhagic retinitis, average systolic blood-pressure . . 205 

3 papillitis, average systolic blood-pressure 225 " 

Slocum has submitted statistics which indicate that many of 
the serious fundus lesions of nephritis are dependent at least in 
part upon some other factor than the angiosclerosis. Similar 
lesions occur in cases showing but little increase in blood-pressure. 

Lenticular Cataract. — What has already been said regarding the 
effect of arterial hypertension in altering the osmotic balance of 
the ocular fluids may in a measure apply to lenticular cataract, 
if we assume that clouding of the lens is due to an abnormal dialysis 
between the anterior and the posterior chambers of this structure. 

1 Reber, W.: A Clinical Study of Ocular Tonometers, Perm. Med. Jour., 1913, 
xvii, 281. 

2 Peter, L. C: Arterial Hypertension and its Relation to Morbid Changes in the 
Eye, Penn. Med. Jour., 1911, sdv, 411. 



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OPHTHALMOLOGY 



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CHRONIC NEPHRITIS 




Fig. 110. — Graphic representation (if totals and percentages in the Table, p. 130. 
Each group represents the percentages of the features as they would appear in an equal 
number of cases: M, male; F, female; /, edema of disk, retina or macula ; -', conges- 
tion or slight swelling of the disk; 3, swelling of disk 1 D, or more; '/, peri-arteritis; 
5, endarteritis; 6, irregular tortuous arteries; 7, silver-wire arteries; 8, cork-screw 
vessels; 9, arteriovenous compression; 10, engorged tortuous veins; 11, periphlebitis; 
12, venous thrombosis; IS, hemorrhages; 1.'+, exudates, etc., retina; 15, retinal detach- 
ments; 16, radiating macular changes; 17, other macular changes; IS, choroidal 
changes; 19, aneurysmal changes. 

Glaucoma. — The general consensus of opinion appears to be that 
arterial hypertension bears only an indirect relation to glaucoma. 
This condition, which is predisposed to by a large lens and a small 
cornea, may be precipitated by a congestion or hemorrhage in the 
ciliary region which interferes with the compensating mechanism. 
"In the former the heightened blood-pressure causes increased 
secretion which in the presence of altered arterial walls is of a 
higher specific gravity than normal, so that the already impaired 
drainage is further embarrassed and compensation fails. In the 
case of hemorrhage, the lymph mixed with blood clogs the outflow 
channels and failure of excretion follows" (Ibershoff). If the 
foregoing facts are accepted, operative measures should not be 
attempted without first lowering arterial pressure, since the opening 
of the anterior chamber or of the sclera would be followed by 
"the rapid reformation of ocular fluids of a much higher specific 
gravity and osmotic coefficient." The danger of expulsive hemor- 
rhage would also be diminished if systemic pressure were lowered. 
Craggs and Taylor, from several hundred comparisons, were unable 
to establish any relations between glaucoma and increased arterial 
tension. 1 McRae's 2 studies of 20 cases lead him to draw similar 
conclusions. 

1 Craggs, H. C, and Taylor, C. G.: A Research into the Relation between Sys- 
temic Blood-pressure and Raised Intra-ocular Tension, Ophthalmoscope, 1913, xi, 350. 

2 Ophthalmoscope, April, 1915, p. 168. 



132 OPKTHALMOLOGY 

Lohlein, 1 who studied some twenty cases of glaucoma by com- 
paring the general blood-pressure, the intra-ocular pressure, and 
the adrenalin content of the blood, was unable to corroborate 
Kleczkowski's statement thai a definite relationship existed. It is 
generally conceded, however, that no study of either acute or 
chronic glaucoma is complete without a record of the systemic 
arterial tension. 

The belief that primary glaucoma is the product of retention 
of intra-ocular volume has been widely accepted. In opposition 
to this hypothesis, Thomas Henderson oilers a different explanation. 
Every ease of primary glaucoma depends upon (1) a constant 
predisposing sclerotic factor, and (2) on the variable vascular factor 
which is directly due to the general circulatory pressure. Since 
neither the eye nor the brain possesses any protective circulatory 
mechanism, "a rise in the vena cava pressure produces, millimeter 
for millimeter, a corresponding and equal rise in intra-ocular and 
intracranial pressures, while increase of pressure in the aorta causes 
a rise of pressure in the eye and brain whose exact amount depends 
on the varying resistance of the arterioles. Glaucoma therefore 
may be caused by a rise of arterial pressure, but is specially to be 
feared when there is a rise of the general venous pressure. This 
in an eye with a sclerotic cribriform ligament, and therefore a 
diminished ^access of aqueous to the veins, precipitates the 
attack. 2 

Retinal Hemorrhages. — Retinal hemorrhages often show a more 
or less direct relation to increase of vascular tension, and ocular 
changes arc most commonly noted in severe cases of nephritis at 
the time at which the pressure is highest. Tims hemorrhages into 
the retina are often precipitated by, and directly attributable to 
conditions which suddenly raise the intracranial arterial pressure, 
such as lifting, stooping, straining, etc. 

The presence of retinal hemorrhages in a case of chronic arterial 
hypertension point almost indubitably to a severe nephritis. 
Retinal changes in nephritis have been reported as follows: Wagner 
in It per cent, of L57 cases, Frerichs in 15 per cent, of 11 cases, 
Lecorche in 22 per cent, of 286 cases, Kales in 28 per cent, of LOO 
cases of chronic kidney disease, Miles Miley in 31 per cent, of 
104 cases of acute and chronic kidney disease, Galezowski in ill 
per cent, of L5 1 cases. 

1 Ueber, Blutuntersuchungen bei Glaucomkranken, Gracfe's Arch. f. Ophthal., 
Ixxxiii, 547. 

• Henderson, Thomas: Glaucoma, London, 1910. 



OCULAR LESIONS AND ARTERIAL PRESSURE 133 

The duration of life after the first retinal changes were noted: Bull 
reported 103 cases: 86 of the patients died, 57 within thefirst 
year, is in the second year, 6 in the third year, \ in the fourth 
year, and I in the sixth year of observation, making 87 per cent, 
in the Qrs1 two years. Miles Miley, in Kil patients with acute 
or chronic kidney disease, found L05 with healthy eyes and 5] with 
retinitis albuminuria (the other 8 had affections of the eyes which 
are not pertinent to our subject); 27 per cent, of the former and 
53 per cent, of the latter died. The mortality shown among those 
having retinitis albuminuria was twice as greal as among patients 
with healthy eyes. Most of the patients lived about twelve months 

after the first indications of retinal changes, two lived nearly 
fourteen months, and one about eighteen months. In those cases 
in which the onset of the retinal disturbance could he definitely 
established the average duration of life did not exceed six months' 
(see page 302). 

The existence of high systemic blood-pressure is of ophthalmo- 
logical interest in relation to postoperative hemorrhage after cataract 
extraction and in spontaneous subconjunctival hemorrhages, although 
the latter may for other reasons occur with normal or even low arte- 
rial tension. The higher the arterial tension, the less favorable is 
the case from an operative stand-point. In such cases vasodilators 
may he administered to reduce pressure during the operation. 
Morphin is also useful, since it helps to prevent the emotional 
disturbance with which a cataract extraction is of necessity asso- 
ciated, and which has such a potent pressor effect. 2 
- Spasm of the retinal arteries of variable duration and of not 
infrequent recurrence is now a well-established ophthalmological 
entity. The vascular spasm has been observed in its incipience 
and disappearance by means of the ophthalmoscope. There seems 
to be a growing conviction that a number of the cases which were 
previously attributed to embolism were really instances of spastic 
arterial contraction. The literature on the subject has been sum- 
marized by Zentmayer, 3 who also reported a case in which he 
repeatedly observed a spasm of the central retinal artery. The 
condition is generally associated with arteriosclerosis and hyper- 



1 Quoted by Posey, W. C. : The Significance of Ocular Findings in Estimating 
Longevity, Jour. Am. Med. Assn., 1913, lx, 1867. 

2 Reber found a rise of pressure of 30 mm. occasioned by the psychic stimulation 
incident to preparation for a cataract extraction. 

3 Some Unusual Ocular Manifestations of Arteriosclerosis, Jour. Am. Med. Assn., 
1906. 

28 



434 OPHTHALMOLOGY 

tension, and causes temporary blindness, usually of the hemianopic 
type (Peter) 1 (sec Vascular Crises, page 264). 

Pulsation of the Retinal Vessels. — Blood-pressure in the oph- 
thalmic artery of animals is only a few millimeters Ilg. below that 
of the carotid. While this relation may not hold good for man, 
arterial pressure is well above the intra-ocnlar tension. Under 
normal conditions the vascular pulsation cannot he ophthalmo- 
scopically demonstrated, probably because the pulsatile movement 
is damped by the intra-ocular tension, and because it is spread 
over the large area of the eyeball. 

Under pathological conditions, aortic insufficiency, aneurysm, 
exophthalmic goitre, etc., arterial pulsation can sometimes be 
seen either as (1) "a true pulse wave, accompanied by locomotion 
of the vessels, and (2) an intermittent flow of blood or pressure 
pulse. In the latter instance, the arteries fill with blood only with 
the heart beats, being empty between them; and pulsation is only 
visible upon the disk. This type of pulsation is a pure pressure 
phenomenon, and is caused by any considerable increase of intra- 
ocular tension with normal or lowered blood-pressure, as in glaucoma 
or by any considerable diminution of blood-pressure with normal 
intra-ocular tension, as in syncope, orbital tumors, etc. The true 
arterial pulse occurs in cases of aortic regurgitation (Quincke) or 
aneurysm, in Graves's disease, etc.; it is not confined to the optic 
disk. It is equally a pressure phenomenon, but the differences of 
pressure are smaller." 

"Capillary pulsation is seen only in aortic regurgitation as a 
systolic reddening and diastolic paling of the disk." Venous pul- 
sation occurs in three forms: (1) the normal negative venous pnlse; 
(2) the positive venous pulse (tricuspid insufficiency), and (3) the 
transmitted centripetal venous pulse (an exaggerated form of the 
normal type due to venous congestion). 2 

A careful ophthalmoscopic examination, in conjunction with 
blood-pressure studies, is therefore often of the greatest value. It 
should be made with a dilated pupil, as minor degrees of vascular 
changes are easily overlooked, but strong mydriatics, such as 
atropin, should not be used on account of the danger of precipita- 
ting an attack of glaucoma. De Schweinitz recommends euph- 
thahnin (3 drops of a 5 to 10 per cent, solution) to be followed after 
the examination by the instillation of a few drops of a solution 
of piloearpin, gr. j to the ounce. 

Arterial Hypertension and its Relation to Morbid Changes in the Eye, Peon. 
Med. Jour., 1911, xiv, 411. 
2 Persons: Pathology of the Eye, 1908, iv, 1254. 



THE EYE-GROUNDS IN ARTERIAL HYPERTENSION 435 

Visual Accommodation. — Systemic blood-pressure also bears a 
relation to visual accommodation which is apt to be better late in 
the day when pressure is at its highest. Hypotensive individuals 
often have less accommodative power. The onset of presbyopia is 
often concomitant with the beginning of arterial hypertension 
(de Schweinitz). Attention has also been called by this eminent 
author to the fact that certain forms of asthenopia, especially those 
occurring in women in the late forties, owe their origin to angio- 
sclerosis, and while rebellious to the usual methods of treatment, 
yield to dietetic and therapeutic measures which tend to lower 
arterial tension. 

A large percentage of the early cases of increased blood-pressure 
are overlooked unless the sphygmomanometer is employed, and 
likewise many cases of incipient arteriosclerosis will not be detected 
if the ophthalmoscope is not called into requisition. This applies 
especially to those cases in which the arterial involvement is chiefly 
cerebral. 

In 90 cases of general arteriosclerosis Rablmann 1 found macro- 
scopic lesions of the vessels of the retina in practically all. Well- 
marked changes occurred in about 20 per cent. 

The Eye-grounds in Arterial Hypertension. — "The eye-ground 
lesions of persistent high arterial tension, when this is a symptom 
of arteriosclerosis, may conveniently be divided into those which 
are suggestive and those which are pathognomonic. The suggestive 
signs include uneven caliber and undue tortuosity of the retinal 
arteries, increased distinctness of the central light streak, and 
unusually light color of the breadth of the artery, and alterations 
in the course and caliber of the veins." 

The pathognomonic signs include changes in the size and breadth 
of the retinal arteries of such character that a beaded appearance 
is produced; distinct loss of translucency ; decided lesions in the 
arterial walls, consisting of white stripes in the form of perivasculitis ; 
alternate contractions and dilatations of the veins, and particularly 
— and this is the most important of the signs — indentation of the 
veins by the stiffened arteries in the same manner as a solid rod 
would indent a rubber tube when lying across it. Sometimes the 
vein is simply flattened slightly at the point of crossing, or merely 
pushed aside, or its caliber is contracted so that beyond the point 
of crossing there is an ampulliform dilatation. In addition to these 
clear signs there may be changes in the venous walls so that they 
are bordered with white stripes. The veins may be exceedingly 

'Quoted by de Schweinitz: Intra-ocular Angiosclerosis and its Prognostic and 
Diagnostic Significance, Internat. Clinics, series 17, i, 177. 



436 OPHTHALMOLOGY 

tortuous and contain varicosities. Finally, there are edema of the 
retina in the form of gray opacity around the disk or following 
the course of the vessels; hemorrhages manifesting themselves as 
linear extravasations or roundish infiltrations, or sometimes assum- 
ing a drop-like form" - (de Schweinitz). ] 

The Ocular Reflex (Aschner). If sufficient pressure is exerted 
upon the eyeball beneath the supra-orbital ridge, the eye being 
turned downward so as to avoid pressure upon the cornea, a reflex 
lowering of the pulse will normally occur. The reflex inhibition, 
as has been experimentally demonstrated, travels over the fifth 
to the tenth nerve. The reflex has been found exaggerated in 
epilepsy, and in exophthalmic goitre. It is not abolished by ether 
anesthesia. It is increased by the administration of pilocarpin 
and diminished by atropin. Considerable pressure is required to 
bring about the reflex, and this in turn entails a good deal of pain 
to the patient and perhaps danger to some eyes. It is not a 
procedure which can be readily or frequently applied, and should 
therefore be reserved for the study of exceptional cases. The 
pressure above mentioned will sometimes slow the pulse when 
direct pressure over the vagus in the neck fails to do so. It is inter- 
esting to remember that Robinson and Draper have shown that the 
right vagus inhibits the heart more than does the left, and similarly 
pressure over the right eye seems to especially exert its effect upon 
the sinus region of the heart, whereas pressure over the left eye seems 
to exert more influence upon the conductive system (Levine). 

The reflex is said to be positive when slowing of the pulse occurs. 
Normally when it occurs the reflex is positive. The absence of 
pulse retardation or an actual increase in rate occurs in sympa- 
thicotonics. In vagotonics, on the other hand, marked slowing 
of the pulse occurs. Indeed, in them pressure maintenance for 
ten to twelve seconds may cause syncope from complete temporary 
asystole. These symptoms are due to an abnormally low nervous 
t lire-hold in the vagus system, since they disappear under atropin. 8 
The claim that the reflex is of diagnostic value in differentiating 
cardiac weakness due to myocardial lesions from those dm- to 
nervous disturbances has not been substantiated. It may be of 
-nine value in differentiating between postfebrile bradycardia and 
auriculoventricular heart-block. 1 This reflex is generally absent 
in tabes dorsalis. 

1 Loc. 'it. 

'NeuRebauer, II.: Beitr. z. Klinik d. Vagotonie, Wien. Win. Wchnschr., 1014, 
xxvii, 1023. 

•Gunson, E. I'..: The Oculocardiac Reflex, British Jour. Child, Dis., 1915, xii, 
No. 136, p. !»7. 



INDEX. 



Abdominal aorta, paroxysmal dilata- 
tion of, -'tis 
Acromegaly, blood-pressure in, 367 
Adams-Stokes syndromes, blood-press- 
ure and, 250 
Addison's disease, blood-pressure in, 

364 
Adiposity, blood-pressure in, 278, 371 
Adrenal glands, physiology of, 35, 290, 
342 
in nephritis, 289 
insufficiency, acute, 399 

white line in, 271 
Age, blood-pressure and, 56 
Aged, blood-pressure in the, 260 
Air, cold, effect on blood-pressure, 213 
Albuminuria, blood-pressure and, 297 

orthostatic, 199 
Alcohol, blood-pressure effects of, 33t> 
Alcoholism, blood-pressure in, 238 
Alkalies, blood-pressure and, 337 
Altitudes, blood-pressure and, •">:;. 373 
Ammonium, blood-pressure effeel <>(, 

337 
Amyloid renal disease, 283 
Anaphylaxis, 219 
Anemia, blood-pressure in, 372 
Aneroid sphygmomanometer, 112 
Anesthesia, blood-pressure during, 423 
chilling during blood-pressure and, 
404 
Anesthetics, blood-pressure and, 408 
Aneurysm, aortic, blood-pressure in, 245 

subclavian, causation of, 246 

Angina abdominalis as vascular crisis, 

267 

pectoris as vascular crisis, 265 

Angioneuroses, blood flow in, 271 

Angioneurotic edema, vascular crises 

and, 271 
Aorta, abdominal, paroxysmal dilata- 
tion of, 268 
Aortic aneurysm, blood-pressure in, 245 
insufficiency, blood-pressure in, 242 
in arm in, 243 
in leg in, 243 
Duroziez's sign of, 245 
Traube's sign of, 245 
obstruction, blood-pressure in, 245 



Aortitis, syphilitic, blood-pressure in, 

222, 298 
Apoplexy, 270, 305, 311, 390 

in vascular crises, 2/0 
Arm. blood-pressure in, in aortic insuffi- 
ciency, 2 13 
estimation of blood flow in, 173 
Arrhythmia, extrasystolic, blood-press- 

u re in. 249 
Arsenic poisoning, blood-pressure in, 

2:« 
Arterial blood-pressure, constitution- 
ally low, L93 
function, estimation of, ISO 
hypertension, 310 
pressure, ocular lesions due to, 429 
tonus, estimation of, 182 

Vries-Reilingh's method, 
182 
Arteries in arteriosclerosis, 261 

coronary, effeel of epinephrin, 342 
effects of alterations of blood-press- 
ure on, 58 
functional tests of, 263 
physiology of, 29 
retinal, blood-pressure in, 425 
pulsation of, 4.'U 

spasm of, 133 
in symptoms of arterial hyperten- 
sion, 279 
Arteriocapillary index in blood-press- 
ure, 264 
Arterioles, effects of alterations of 
blood-pressure on, 58 
physiology of, 30 
Arteriosclerosis, arteries in, 261 

bilateral variations of pressure in, 

261 
blood-pressure in, 258 

in tobacco poisoning, 235 
ice reaction in, 263 
nitrite test of, 263 
stasis reaction in, 263 
vascular reactions in, 261 
Aspiration of pleura, blood-pressure 

effect of, 406 
Asthma, bronchial, blood-pressure in, 

257 
Athletics, blood-pressure and, 49, 154, 

315, 382 
Atropin, blood-pressure effect of, 337 



438 



INDEX 



Aura] symptoms of arterial hyperten- 
sion. 279 

Auricular fibrillation, blood-pressure in. 
250 

Auscultatory determination of blood- 
pressure, '-'-':; 
phases, duration of, 213 

Auto-intoxication, blood-pressure in, 
365 

Aviation, circulatory symptoms in, 205 



B 



Bajabdi's ocular sphygmojnanometer, 

426 
Barach's formula of blood-pressure 

quotient, 168 
Barometric pressure, 375 
Benedick's sphygmomanometer, 86 
Berberin, blood-pressure effect of, 346 
Bichloride of mercury poisoning, 307 
Biliary colic and vascular crisis, 269 
Bine's sphygmomanometer, L09 
Birth, bloocUpressure at, 378 
Bishop's sphygmomanometer, 82 
Bladder drainage, effect on blood-press- 
ure, 407 
Bleeding. See Hemorrhage, phlebot- 
omy, 326, 372, 400 
Blood and blood-pressure, 36 
flow in angioneuroses, 271 
blood-pressure and, 37 
estimation of, 170 
in arm, 173 

Bornstein's method, 178 
dynamic diagrams in, 187 
Fellner's method, 178 
Hewlett's method, 177 
Stewart's method, 170 
plethysmography in, 173 
tachograph in, 180 
Van Zwaluwenburg's 

method, 177 
von Rries's method, 180 
in fevers, 205 
renal function and, 292 
systolic output, estimation of, by 
venous pressure, 171 
Blood-pressure, absolute Bphygmogram 
in, 164 
in acromegaly, 3(17 
in acute endocarditis, 241 
nephritis. 306 

in Adams-Stokes syndromes, 250 

in Addison's disease, 364 
in adiposity, 278, 371 
age and, 56 
in aged, 260 
albuminuria and, 297 
alcohol and. 336 
in alcoholism, 238 

alkalies and, 337 



Blood-pressure, alterations of, effects 
of, on arteries, 58 
on arterioles, 58 
on capillary pressure, 58 
on heart, 57 
on kidneys, 59 
on organs of body, 57 
on pulmonary pressure, 58 
on venous pressure, 58 

altitudes and, -53, 373 

ammonium and, 337 

in anemia, 372 

anesthetics and, 423 

in aortic aneurysm, 245 
insufficiency, 242 
obstruction, 245 

in arm, in aortic insufficiency, 242 

in arsenic poisoning, 235 

arterial, constitutionally low, 193 

arteriocapillary index, 264 

in arteriosclerosis, 258 

in aspiration of pleura, 406 

athletics and, 49, L54, 316, 382 

atropin and. '■)'■'>< 

in auricular fibrillation, 250 

in auto-intoxication, 365 

bandaging of extremities and, 327 

and barometric pressure, 375 

berberin and, 346 

in bichloride of mercury poisoning, 
307 

at birth, 378 

blood in, 36 

flow and, 37 

in bradycardia, 250 

bromides and, 342 

in bronchial asthma , 257 

in cachexia, 373 

caffein and, 338 

camphor and, 339 

capillary, estimation of, 183 

in carcinoma, 373 

cardiac cycle in, 25 

in cardiac disease, 240 

in cerebral hemorrhages, 389 

chemical regulation of, 35 

in Cheyne-Stokes respiration, 300 

in childhood, 56, 377 

chilling during anesthesia and, 404 

chloral and, 342 _ 

after chlorin-gas inhalation, 235 

chloroform and, 408 

in chlorosis, M72 

in cholera, 207 

and climate, 375 

cocain and, 410 

in collapse, 219 

counter-irritation and, 331 

cuff, ()2 

location of, 65 

in delirium tremens, 238 

in dementia precox, 388 

in diabetes, 360 



INDEX 



439 



Blood-pressure, diastolic, 39, 134, 274 
diel and, 317 
digestion, effect of, 52 
digitalis and, 339 
in diphtheria, 207 
in diseases of heart, 240 

of myocardium, 249 

of nervous system, 386 
during anesthesia, 123 
and dysmenorrhea, 417 
in eclampsia, 421 
edema and, 248 
electricity and, 328 
in encephalopathy, 234 

treatment of, 235 
in epilepsy, 388 
epinephrin and, 342 
ergol and. 3 I I 

erythrol tetranitrate and, 350 
estimation of, 61 

accuracy of, 133 

auscultatory, 69 

graphic method of, 87 

instrumental, 61 

oscillatory method of, 10S 

palpatory, 65 

personal equation of examiner 
in, 131 

possible accidents in, 133 

precautions in, 129 

sources of, error in, 126 

subjective method of, 123 

technic of, 129 

value of, 133 

visual method of, 108 
ether and, 408 
ethyl chloride and, 40'.) 
exercise and, 41), 155, 3 Hi. :;s2 
in exogenous intoxications, 232 
in exophthalmic goitre, 367 
in extrasystolic arrhythmia, 249 
in extra-uterine pregnancy, 422 
extremes, compatible with life, 136 
factors maintaining, 24 

regulating, 24 
feeding and, 52 
fluid intake and, 320 
fresh air and, 213 
in gastro-enteritis, 385 
glandular extracts and, 366 
in glaucoma, 431 
gonads, effect of, 419 
in gout, 363 
normal and, 346 
heart in, 25 
in heart-block, 250 
in hemiplegia, 391 
in hemorrhage, 372, 400 
in hemorrhages of brain, 389 
hemic viscosity and, 308 
hydrastinin and, 346 
hydrastis and, 345 
hydrotherapy and, 320 



Blood-pressure in hydrothorax, 230 
in hyperemesis gravidarum, 422 
hyperglycemia and, 295, 360 
in infants, 377 
in infectious diseases, 204 
acute, 207 
chronic, 222 
treatment of, 217 
instruments, choice of, 137 

classification of, 139 

different types of, 139 

graphic registration, 92 
intra-abdominal, 44 

estimation of, 191 

Moritz's method, 191 

increased, 268 
intracranial, 45 
intra-ocular, 46 
intrapcricardial, 44 
iodides and, 346 
in jaundice, 364 
kidneys and, 284, 296 
in lead poisoning, 232 
in leg, in aortic insufficiency, 243 
in lenticular cataract, 429 
life insurance and, 376 
in locomotor ataxia, 392 
in lumbar puncture, 411 
lymph flow and, 36 
in malaria, 209 

manipulations of pelvic viscera 
and, 405 

of thoracic viscera and, 405 
mannitol nitrate and, 350 
massage and, 330 
maximum, 22 
mean, estimation of, 39 
measurement of, method of, 19 
in meningitis, cerebrospinal, 210 

tuberculous, 210 
in menopause, 418 
in menstruation, 417 
in mental diseases, 387 
in mercurial poisoning, 307 
in metabolic diseases, 360 
minimum, 22 
mistletoe and, 347 
in mitral insufficiency, 246 

obstruction, 248 

stenosis, 248 
morphin and, 351 
in morphinism, 239 
muscular exertion in, 50, 155, 316, 

382 
in myxedema, 371 
Nauheim baths and, 321 
neosalvarsan, 355 
in nephritis, 281 
in neurasthenia, 386 
in neuroses, 386 
nitrites and, 347 
nitrogen retention and, 295 
nitroglycerin and, 349, 350 



440 



INDEX 



Blood-pressure, nitrous oxide and, 109 
normal, 56, 378 

rule for estimating, :'>77 
in obstetrics, 39 I 
ocular tension and, 12."> 
in old age, 260 
in ophthalmology, 125 
opium and, 351 

orthostatic albuminuria and, 199 
pancreas extracl and, 289 

in paracentesis al idoiiiinalis, l<)!> 

para-oxyphenylethylamin ami. :; 15 

in paratyphoid lexer. 215 

in paresis. 393 

m paroxysmal dyspnea, 298 

passive change of posture in. 154 

pedial rics and. :;77 

in pericardial effusions, 256 

phlebotomy am!, :i27 

in phosphorus poisoning, 235 

physical efficiency ami. :;7'.> 

pituitary extracl ami. 352 

in pleural effusions, 229 

in pneumonia, 21 1 

in pneumothorax, 230 

in polycythemia, :!<>7 

postural response in, 152 

posture and, 51 

patient and, 403 
in pregnancy, 419 
at puberty, 378 
in pulmonary edema, ^01 

hemorrhage, 227 
pulse, 40 

in pulsus alternans, 250 
purgation and, 314 
quotient, 165 

Barach's formula, 168 

Erlanger and Hooker's for- 
mula, 167 

Fuerst and Soetbeer's for- 
mula, 167 

Tigerstedt formula, 166 

von Recklinghausen's for- 
mula, 1,68 
radio-act ive substances in, 333 
renal decapsulation and, :;:;."") 
i< pirat ion and, 40 
m retinal artenes, 125 

hemorrhages, 432 

-al \ar-ai) and. '■','• 1 
in scarlet fever, 2 1 1 
secrel ion and, 19 

of urine and, 296 
m senility, 260 
in shock, 21 ( .) 

treatment of, 220 

significance of, 137 
3I1 ep ami, .".:;, 315 
in smallpox, 215 

3odium chloride metabolism and, 
296 

mt rite and, 350 



Blood-pressure in spinal anesthesia, 112 
in status lymphaticus, .'571 
si rophanthua and. 353 
strychnin and, 355 
in Burgery, 39 I 
in surgical honiorrhage, 400 

shock. 396 
in syphilis, 222 
in syphilitic aortitis, 298 

myocarditis, 249 
in syringomyelia, 393 
systolic, :;'.) 

in tachycardia. 250 

paroxysmal, 250 

testes and. 419 

throughout vascular tree. 23 

t nyroid extract and, 355 

tissue extracts and. 366 

in tobacco poisoning, 2:1.1 

arteriosclerosis and, 237 
tropical climates and, 375 
in tuberculosis, 223 
in tumors of brain, 389 
in typhoid fever, 215 
in uremia, 298 
urethane and, 356 
vasotonin and, 356 
venous, 23, 27 

in shock, 398 
visceral manipulations and, 404 
visual accommodation and, 435 
yohimliin and, 356 
Bloodvessels, resistance of, estimation 

of, 180 
Bornstein's method of estimation of 

blood flow, 178 
Bouloumie's sphygmomanometer, 123 
Bradycardia, blood-pressure in, 250 
Brain, hemorrhages of, blood-pressure 
in, 389 
tumors of. blood-pressure in, 389 
Bromides, blood-pressure and, 342 
Bronchial asthma, blood-pressure in, 

257 
Brugsch's sphygmomanometer, 102 
Bussenius's sphygmomanometer, 106 



Cachexia, bl l-pressure in, 373 

( laffein, blood-pressure and, :;:;s 

Camphor, blood-pressure and, .'!:!!• 

( 'apillaries. physiology of, 30 

( 'apillarv blood-pressure, estimation of, 
1 11. ls:i 
pressure, effects of alterations of 
arterial pressure < n, 58 

Carbon monoxide poisoning, blood- 
pressure in. 239 

Carcinoma, blood-pressure in, :;7:J 
Cardiac action, venous pressure and, 
149 



/ \ BEX 



441 



Cardiac cycle and blood-pressure, 25 
disease, blood-pressure in, 210 
Load, 273 

rate, 28 
lone, 28 

Cardiovascular disease, arterial hyper- 
tension in, 274 
symptoms in arterial hypertension, 
278 
Cataract, lenticular, blood-pressure in, 

429 
( Jerebral hemorrhages, blood-pressure 
in, 389 
vascular crises, 269 
( lerebrospinal meningitis, blood-press- 
ure, 210 
pressure in blood-pressure. 390, 112 
( !ervical rib, effect on M l-pressure in 

the arm, 246 

Chemical regulation of blood-pressure, 
35 

( Jheyne-Stokes respiration, Mood-press- 
ure in, 300 
Chilblains, vascular crises and, 271 
Childhood, blood-pressure in. .'177 

Chloral, blood-pressure effed of, 342 
Chlorin-gas poisoning, 235 

Chloroform, blood-pressure effect of, 
Ids 
in pulmonary hemorrhage, 228 
Chlorosis, 372 

Cholera, blood-pressure in, 207 
Cholesterinemia and hypertension, 290 
Christen's energometer, 190 
Circulation, functional efficiency of, 151 
amplitude frequency pro- 
duct of, 168 
( Jrampton's table of, 152 
energy index in. 168 
( traupner's test of, 157 
Katzenstein's test of, 161 
Claudication, intermittent, in vascular 

crises, 270 
Climate, 375 

Cocain, blood-pressure effect of, 410 
Colic, biliary, in vascular crises, 269 

renal, in vascular crises, 269 
Collapse, blood-pressure in, 219 
Conduction of pulse waves, 128 
Coronary arteries, effect of drugs on, 

357 
Corpulence, 278, 371 
Cramps in the legs, treatment of, 273 
Crampton's table of functional effi- 
ciency of circulation, 152 
Critical venous pressure, 26 
Cuff, blood-pressure, 62 



Decompensation and venous blood- 
pressure, 341 



Delirium tremens, blood-preseure in, 

238 
Dementia precox, blood-pressure in, 388 
Depressor nerve, physiology of, :-;:; 
Dermographism, vascular crises and, 

271 
1 )iabetes, blood-pressure in. 360 
I >iastole, I ime relal ions of, 25 

I Lie pressure, definition of, 17 

estimation of, r,7, 125 
by palpal ion, lis 

significance of, 13 I 

by visualization, lis 
Diet, blood-pressure ami, :!17 

in hypertension, 317 

Digestion, effect on blood-pressure, 52 

Digitalis, blood-pressure effecl of, 339 
in failing compensation, 3 10 
in high-pressure stasis, 340 
in pulmonary hemorrhage, 227 

Dilatation, paroxysmal, of abdominal 
aorta, 268 

Diphtheria, blood-pressure in, 207 

Dysmenorrhea and Mood-pressure, 417 
Dyspnea, paroxysmal, Mood-pressure 

in, 2'. is 
Drugs, effects of, on blood-pressure. 336 
on coronary arteries, 357 
on vasomotor system, 220 
on venous pressure, 358 
Duroziez's sign of aortic insufficiency, 

245 
Dynamic diagrams in estimation of 
blood flow, 187 



Eclampsia, blood-pressure in, 421 
Edema, angioneurotic, vascular crises 
and, 271 

blood-pressure and. 2 Is 

pulmonary, blood-pressure in, 301 

sodium chloride and, 296 
Ehret's phenomenon, 68 
Electricity, blood-pressure and, 328 
Encephalopathy, blood-pressure in, 234 
End pressure, definition of, 18 
Endocarditis, acute, blood-pressure in, 

241 
Energometer, Christen's, 190 
Energy index in functional efficiency 

of circulation, 168 
Enteroclysis in hypertension, 315 
Epilepsy, blood-pressure in, 388 
Epinephrin, blood-pressure and, 35, 342 
Ergot, blood-pressure and, 344 

in pulmonary hemorrhage, 228 
Erlanger and Hooker's formula for 

blood-pressure quotient, 167 
Erlanger's sphygmomanometer, 96 
Erythrol tetranitrate, blood-pressure 
and, 350 



442 



INDEX 



Erythromelalgia, 27(» 

Kther, blood-pressure effect of, 10s 

Ethyl chloride, blood-pressure effect of, 

ll'l'.l 

Exercise, blood-pressure and, 49, 155, 
316, 382 

Exogenous intoxications, blood-press- 
ure in, 232 

Exophthalmic goitre, blood-pressure in, 
367 

Extrasystolic arrhythmia, blood-press- 
ure in. 2 I'.' 

Extra-uterine pregnancy, blood-press- 
ure in. 422 

Eye-grounds in arterial hypertension, 



Fasting, effect on blood-pressure, 317 
Faught's sphygmomanometer, 78 
Fedd6's oscillometer, 1 10 
Feeding, blood-pressure and, 52 
Fellner's method of estimation of blood 

flow, 178 
Fevers, blood flow in, 205 
Fibrillation, auricular, blood-pressure 

in, 250 
Fibromyomata uteri, blood-pressure 

and, 423 
Finger plethysmograph, Fleischer's, 175 
Fleischer's finger plethysmograph, 175 

sphygmomanometer, 105 
Fluid intake, blood-pressure and, 320 
Francois Frank's sphygmomanometer, 

123 
Frank and lleh's method of estimation 

of venous pressure, 142 
Frey's method of estimation of venous 

pressure, 141 
Fuerst and Soetbeer's formula of blood- 
pressure quotient, 167 
Function, arterial, estimation of, 180 
Functional capacity of heart, 151 
efficiency of circulation, 151 
hypotension, 240 
tests of arteries, 263 



G&BTNEb's method of estimation of 
venous pressure, 140 
phenomenon, 140 
sphygmomanometer, 80 

enteritis, Mood-pressure in, 385 
Gastro-intestinal symptoms of arterial 

hypertension, 278 
( ribson's sphygmomanometer, 93 
( tlandular extracts, blood-pressure and, 
366 

< llaiiconia, Mood-pressure, in, 431 

< roit re, exophthalmic, 367 



Gonads, effect on blood-pressure, 36, 

419 
Gout, Mood-pressure in, 363 
Graphic method of estimation of blood- 

pressure. S7 
Graupner's test of functional efficiency 
of circulation, 157 



Heart and blood-pressure, 25 

block, blood-pressure and, 250 
diseases of, blood-pressure in, 240 
effects of alterations of blood- 
pressure on, 58 
functional capacity of, 151 
symptoms of arterial hyperten- 
sion, 279 
work done by, 310 
Heat and cold applied to the abdomen, 

415 
Hemic viscosity, blood-pressure and, 

308 
Hemiplegia, blood-pressure in, 391 
Hemoglobinuria, vasomotor, 201 
Hemorrhage, blood-pressure in, 372, 400 
Hemorrhages of brain, blood-pressure 
in, 389 
pulmonary, blood-pressure in, 227 
retinal, blood-pressure in, 432 
surgical, blood-pressure in, 400 
Hertz's sphygmomanometer, 85 
Hewlett's method of estimation of 

blood flow, 177 
Hill's sphygmomanometer, 77 
Hooker and Eyster's method of estima- 
tion of venous pressure, 142 
Hormonal, blood-pressure and, 346 
Howell's method of estimation of ven- 
ous pressure, 142 
Htirthle's manometer, 20 
Hydrastinin, blood-pressure effects of, 

346 
Hydrastis, blood-pressure effects of, 345 
Hydrotherapy, blood-pressure and, 320 
Hydrothorax, blood-pressure in, 230 
Hyperemesis gravidarum, blood-press- 
ure in, 422 
Hyperglycemia and hypertension, 295, 

360 
Hyperpiesis, 281 
Hypertension, arterial, 310 

bandaging of extremities in,327 
blood volume in, 275 
in cardiovascular disease, 310 
cholesterinemia and, 200 
climate in, 332 
complications of, 298 
conservation of energy in, 319 
counter-irritation in, 331 
diet in, 317 
electricity in, 328 



INDEX 



143 



ll> pertension, arterial, exorcise in, 316 
eye-grounds in, 435 
fluid intake in, 320 
hemic viscosity and, 308 
hydrotherapy in, 320 
massage in, 330 
Nauheim baths in, 32] 
phlebotomy in, 327 
prognosis of, 302 
radio-active .substances in, 333 
respirator} gymnastics in, 332 
retinal hemorrhages in, 132 
specific treatment in, 222 
surgical I reatmenl in, 335 
symptoms of, 27s 
arteries, 279 
aural, 279 
cardiovascular, 278 
gastro-intestinal, 278 
heart in, 279 
nervous, 278 
ocular, 278 
renal, 278 
signs in, 279 
treatment of, 310 
psychic, 332 
hyperglycemia and, 295, 360 
in nephritis, 281 
etiology of, 283 
symptoms of, 282 
nitrogen retention and, 295 
renal circulation and, 292 

function and, 292 
secretion of urine in, 293 
viscosity and, 308 
Hyperthyroidism, 367 
Hypnosis, 156 
Hypotension, 193 
causes of, 193 
etiology of, 196 
extreme, prolonged, 373 
functional, 240 
in lumbago, 201 
mechanical, 240 
in myalgia, 201 
in neuritis, 201 
in phosphaturia, 201 
in rheumatoid arthritis, 201 

treatment of, 201 
in sciatica, 201 
in status lymphaticus, 201 
symptoms of, 193 
terminal, 240 
treatment of infectious disease, 217 



Infectious diseases, blood-pressure in, 
204 
venous pressure in, 207 
Insufficiency, mitral, blood-pressure in, 
246 



Intermittent claudication, 270 
Intoxications, exogenous, blood-press- 
ure in, 232 
Intra-abdominal pressure, 44 
estimation of, 191 
increased, 268 
lnt racranial blood-pressure, 45 
[ntra-ocular blood-pressure, 46 

pressure, venous pressure and, 427 
tension, estimation of, 428 
1 nt r;i pericardial blood-pressure, 44, 256 
I lit in venous injection, venous pressure 

and, 150 
Iodides, blood-pressure and, 346 



Jacquet's sphygmotonograph, 92 
Janeway's sphygmomanometer, 76 

Jaundice, blood-pressure in, 364 



Katzenstein's test of functional effi- 

ciency of circulation, 161 
Kidney, decapsulation and blood-press- 
ure, 335 
Kidneys, amyloid disease of, 283, 286 
blood-pressure and, 283, 287 
effects of alteration of blood-press- 
ure on, 59, 292, 296 
nephritis, 2S3, 286 
tuberculosis of, 283 



Lateral pressure, definition of, 18 
Lead poisoning, blood-pressure in, 232 
Leg, blood-pressure in, in aortic insuffi- 
ciency, 243 
Lenticular cataract, blood-pressure in, 

429 
Life insurance, blood-pressure and, 376 
Locomotor ataxia, blood-pressure in, 

392 
Lumbago, hypotension in, 201 
Lumbar puncture, blood-pressure in, 

411 
Lymph circulation and in blood-press- 
ure, 36 



M 



Malaria, blood-pressure in, 209 
Malingering, detection of, 386 
Mannitol nitrate, blood-pressure effect 

of, 350 
Manometer, Hurthle's, 21 
maximum, 22 



411 



INDEX 



Manometer, mercury, 19 

minimum, 22. S, , Sphygmoman- 
ometer. 
Manometers, spring, in estimation of 

venous pressure. 140 
Massage, blood-pressure and. 330 
Mean pressure, definition of, 17 

rule for estimating, 39 
Mechanical hypotension, 2 lit 
Meningitis, cerebrospinal, blood-press- 
ure in. 210 
tuberculous, blood-pressure in, '-'lit 
Menopause, blood-pressure in, 1 In 
Menstruation, blood-pressure during, 

117 
Menial diseases, blood-pressure in, 38< 

work, physiology of, 33 
Mercer's sphygmomanometer, 76 
Mercurial poisoning, blood-pressure in, 

307 
Mercury manometer, 19 
Metabolic diseases, blood-pressure in, 

360 
Metabolism, sodium chloride, blood- 
pressure and, 296 
Mistletoe, blood-pressure and, 347 
Mitral insufficiency, blood-pressure in, 
246 
obstruction, blood-pressure in, 248 
stenosis, blood-pressure in, 248 
Momburg's bell constriction, 414 
Moritz and Tabora, intravenous needle 
of, in estimation of venous pressure, 
143 
Moritz's method of estimating intra- 
abdominal pressure, 191 
Morphin, blood-pressure and, 351 
Morphinism, blood-pressure in, 239 
Muenzer's sphygmomanometer, 103 
Muscular exertion in blood-pressure, 

50, 155, 316, 382 
Myalgia, hypotension in, 2Q1 
Myocarditis, syphilitic, 249 
Myocardium, blood-pressure in diseases 

of, 249 
Myofibroma, blood-pressure and, 423 
Myxedema, blood-pressure and, '47\ 



N 



Nauheim baths, blood-pressure effects 

of, 321 
Neosalvarsan, effeel on blood-pressure, 

355 
Nephril is, acute, blood-pressure in, 306 

chronic, blood-pressure in, 281 

hj pertension in, 281 

NsrV< depressor, phySlolcgl ■'!' 

Nervous Bymptoms of arterial hyper- 
tension, 278 
system, diseases of, blood-pressure 
in, 386 



Neurasthenia, blood-pressure in, 386 
Neuritis, hypotension in. 201 
Neuroses, blood-pressure in, 386 
Nicholson's sphygmomanometer, 74 
Nitrite test of arteriosclerosis, 263 

Nit rites, hi l-pressure and. 3 17 

in pulmonary hemorrhage, 228 
Nitrogen retention and blood-pressure, 

295, 297 _ 
Nitroglycerin, blood-pressure effects of, 

349, 350 
Nitrous oxide, blood-pressure and, lu'.t 

Normal arterial bl l-pressure, 56, 378 

venous blood-pressure, 1 17 



( Obstetrics, blood-pressure in, 394 

Obstruction, aortic, blood-pressure in, 
245 
mitral, blood-pressure in, 248 
Ocular sphygmomanometer, Bajardi's, 
426 
Rubino's, 42(1 
symptoms of arterial hypertension, 
278 
Old age, blood-pressure during, 260 
( (liver's sphygmomanometer, 85 
Ophthalmology, blood-pressure in, 125 
Opium, blood-pressure and, 351 
Orthostatic albuminuria, 199 

blood-pressure and, 199 
Oscillations of first order, 17 
of second order, 17 
of third order, 18 
Oscillatory method of estimation of 

blood-pressure, 108 
Oscillomanometer, Widmer, 112 
Oscillometer, Fedde's, 110 
Ovaries and vasomotor reactions, 418 



Pachon's sphygmomanometer, 112 
Palpatory estimation of blood-pressure, 
65 

Pal's sphygmoscope, 108 
Pancreas extract, effect on blood-press- 
ure, 289 
Paracentesis abdominal is, blood-press- 
ure effects of, 406 
Paratyphoid fever, blood-pressure in, 

215 
Paresis, blood-pressure in, 393 
Para-oxyphenylethylamin, blood-press- 
ure and, 345 
Paroxysmal dilatation of abdominal 
'aorta, 268 
dyspnea, blood-pressure in. 298 
tachycardia, blood-pressure in. 2'A) 

Pediatrics, blood-pressure and. 377 



INDEX 



445 



Pelvic viscera, manipulations of, and 

blood-pressure, 405 
Periarteritis nodosa, 371 
Pericardial effusions, blood-pressure in, 

256 
Phases, auscultatory, 213 

relai ive duration of, 213 
Phenomenon, ( lartner's, 140 
Phlebotomy, blood-pressure and, 227, 

327, 394 
Phosphaturia, hypotension in, 201 
Phosphorous poisoning, blood-pressure 

in, 235 
Physical efficiency and blood-pressure, 

379 
Physiology of arteries, 29 
of arterioles, 31 
of capillaries, 30 
of depressor nerve, 33 
of mental work, 33 
of vasoconstrictor system, 32 
of vasodilator nerves, 3 I 

system, 34 
of vasomotor system, :;i 
of veins, 30 
Pilocarpin, 352 
Pituitary extract, blood-pressure an 1. 

352 
Pituitrin in pulmonary hemorrhage, 22s 
Plethysmograph in estimation of blood 
flow, 173 
Fleischer's finger, 17f> 
Pleura, aspirati n i f. effect on blood- 
pressure, 106 
Pleural effusions, blood-pressure in, 229 
Pneumonia, blood-pressure in, 211 
Pneumothorax, blood-pressure in, 230 
Poisoning, arsenic, Mood-pressure in, 
235 
lead, blood-pressure in. 232 
mercurial, blood-pressure in, 307 
phosphorus, blood-pressure in, 235 
tobacco, blood-pressure in. 235 
Polycythemia, blood-pressure in, 307 
Postural response in blood-pressure, 152 
Posture, blood-pressure and, 51 

effect on readings from right and 

left arm, 155 
passive change of, 154 
Potain's sphygmomanometer, 122 
Pregnancy, blood-pressure and viscos- 
ity, 309 
extra-uterine, blood-pressure in, 

422 
normal, blood-pressure in, 419 
Pressure, diastolic, definition of, 17 
lateral, definition of, 18 
mean, definition of, 17 

estimation of, 39 
normal, 56, 378 
pulse, definition of, 17 
systolic, definition of, 17 
venous, 140 



Puberty and blood-pressure, 378 
Pulmonary artery, effeel of A\\i<^ upon, 
359 
edema, blood-pressure in, 301 
hemorrhage, Mood-pressure in, 227 
chloroform in, 228 
digitalis, 227 
ergot in. 228 
nitrites in, 228 
pituitrin in, 228 
treatmeni of, 227 
pressure, effects of alterations of 
Mood-pressure on, 58 
Pulse, Mood-pressure and. 10. 253 

deficit, 251 

pressure, definition of, 17 

urinary secretion and, 293,296 

r&nge of, lo 

significance of, 134 

waves, c luction of, 128 

Pulsus alternans, Mood-pressure ill. 250 

paradoxus, 107, 256 
Purgation, blood-pressure and, 314 



Radio-active substances effect on 

Mood-pressure. 333 

Raj naud's disease, 270 
Reflex, ocular, 136 

Renal circulation, hypertension and, 
202 
colic in vascular crises, 269 
function, Mood How and, 292 

hypertension and. 202 
symptoms in arterial hypertension, 
278 
Respiration, blood-pressure and, 40 
Cheyne-Stokes, blood-pressure in, 

300 
venous pressure and, 149 
Retinal arteries, blood-pressure in, 425 
pulsation of, 434 
spasm of, 433 
hemorrhages, blood-pressure in, 432 
Rheumatoid arthritis, hypotension in, 

201 
Rib, cervical, producing subclavian 

aneurysm, 246 
Riva-Rocci type of sphygmomanom- 
eter, 65 
Rubino's ocular sphygmomanometer, 
425 



Sahli's sphygmobolometer, 186 
Salvarsan, blood-pressure and, 354 
Scarlet fever, blood-pressure in, 214 
Schiotz's tonometer, 428 
Schott's test by venous pressure, 163 



146 



INDEX 



Sciatica, hypotension in, 201 
Scurvy. 371 

Secretion, blood-pressure and, 49 
Senility, blood-pressure in. 260 
Shock, blood-^reesure in, 219, 396 

medical <>r toxic, 219 
Significance of blood-pressure changes, 

[33 
Silbermann's sphygmomanometer, 101 
Singer's sphygmomanometer, 96 
Sleep, blood-pressure and, 53, 315 
Smallpox, Mood-pressure in, 215 
Sodium chloride, edema and, 296 

metabolism, blooi 1-pressure 
and, 296 

nitrite, blood-pressure and, 350 
Spasm of retinal arteries, 433 
Sphygmobolometer, 184 
Sphygmogram, absolute, in blood- 
pressure, 164 
Sphygmomanometer, aneroid, 112 
standardization of, 119 

classification of, 139 

compressed-air, 85 

Bendick's, 86 

Bing's, 108 

Bishop's, 82 

Bouloumie's, 123 

Brugsch's, 102 

Bussenius's, 107 

Erlanger's. 96 

Faught's, 78 

Fleischers, 105 

Francois Frank's, 123 

( iartner's, 80 

Gibson's, 93 

I Eertz's, 85 

Hill's, 77 

Janeway's, 76 

McKesson's, 423 

.Mercer's, 76 

Muenzers, 103 

Nicholson's, 74 

ocular, Bajardi's, 426 
lb il >ino's, 425 

< Hiver's. 85 

Pachon's, 112 

Potain's, 122 

Riva-Rocci type of, 65 

Silbermann's, 101 
Sphygmomanometer, Singer's, 96 

Stanton's, tit; 

Tycos, 116 

Uskoff's, 98 

Van Westenrijk's, 82 

Vaquez's, 1 12 

von Recklinghausen's, 1 L9 

\\i« liner's, 112 

WybaWs, 108 
Sphygmomanometers, comparative 

values of, 12 1 
Sphygmoscope, Pal's, L08 
Sphygmotonograph, Jacquet's, 92 



Spinal anesthesia, blood-pressure in, 412 

Standardization of aneroid sphygmo- 
manometer, 119 

Stanton's sphygmomanometer, 66 
Stasis, high-pressure, 241, 277, 326, 340 

digitalis in, 340 
Status Ivmphatieus, blood-pressure in, 
371 
hypotension in, 201 
Stephenson's tonometer, 428 
Stewart's method of estimation of 

blood flow, 170 
Strophanthus, blood-pressure effect of, 

353 
Strychnin, blood-pressure effect of, 355 
Subjective method of estimation of 

blood-pressure, 123 
Suckling, effect of, on blood-pressure, 

378 
Suprarenal glands, physiology, 35, 290, 

342 
Surgery, blood-pressure in, 394 
Surgical hemorrhage, blood-pressure in, 
400 
shock, blood-pressure in, 396 
treatment of, 401 
Syphilis, blood-pressure in, 222 
Syphilitic aortitis, blood-pressure in, 

222, 298 
Syringomyelia, blood-pressure in, 393 
Systole, time relations of, 25 
Systolic blood-pressure, 39 
output, 27, 134 
pressure, definition of, 17 
estimation of, 65 



Tabes dorsalis, 392 
Tache cerebrate, 271 
Tachograph in estimation of blood 
flow, 180 
von Kries, 180 
Tachycardia, blood-pressure in, 250 
Terminal hypotension, 240 
Testes, effect of, on blood-pressure, 419 
Thoracentesis, effect of, on blood-press- 
ure, 405 
Thoracic viscera, manipulations of, and 

blood-pressure, 405 
Thyroid extract, blood-pressure and, 

355 
Tigerstedt's formula of blood-pressure 

quotient, L66 
Tissue extracts, Mood-pressure and, 366 
Tobacco poisoning, blood-pressure in, 

235 
Tonometer, Gartner's, 80 
Schiotz's, 428 
Stephenson's, 428 
von Recklinghausen's, 1 19 
Tonus, arterial, estimation of. L82 



INDEX 



117 



Toxemia, alimentary, 365 

Training, effect of, on blood-pressure, 

385 
Traube-Herring waves, 43 
Traube's sign in aortic insufficiency,245 
Tropical climates, blood-pYessure and, 

375 
Tuberculosis, blood-pressure in, 223, 

of kidney, 283 
Tuberculous meningitis, blood-pressure 
• in, 210 

Tumors of brain, blood-pressure in, 389 
Tycos sphygmomanometer, 116 
Tympanites in vascular crises, 268 
Typhoid fever, blood-pressure in, 215 
inoculation, low blood-pressure 
after, 217 
Tyramin, blood-pressure effect of, 203 



Uranium nephritis, blood-pressure in, 

295 
Uremia, blood-pressure in, 298 
lumbar puncture in, 313 
venesection in, 313 
Urethane, blood-pressure and, 356 
Urine, secretion of, blood-pressure and. 
296 
in hypertension, 293 
Urticaria, vascular crises and, 270 
Uskoff's sphygmomanometer, 98 



Van Westenrijk's sphygmomanom- 
eter, 82 
Van Zwaluwenburg's method of estima- 
tion of blood flow, 177 
Vaquez's sphygmomanometer, 112 
Vascular crises, 264 

angina abdominalis in, 267 
pectoris in, 265 

angioneurotic edema and, 271 

apoplexy in, 270 

biliary colic in, 269 

cerebral, 269 

chilblains and, 271 

in children, 271 

compensation, 280 

dermographism and, 271 

epilepsy and, 269, 388 

intermittent claudication in, 
270 

in locomotor ataxia, 392 

peripheral, 270 

renal colic in, 269 

treatment of, 273 

tympanites in, 268 

urticaria and, 271 

vasoconstriction and, 265 



Vascular crises, vertigo in, 269 

reactions in arteriosclerosis, 26] 
tonus, estimation of, 182 
tree, blood-pressure throughout, 23 
Vasoconstriction, vascular crises and, 

265 
Vasoconstrictor system, physiology of, 

32 
Vasodilator nerves, physiology of, 34 
system, physiology of, '■> I 
therapeusis, 220 
Vasomotor centre, effect of drugs upon, 
220, 359 
efficiency test, 152 
system, physiology of, 31 
Vasotonin, blood-pressure and, 356 
Veins, physiology of, 30 
Venesection, effect on blood-pressure, 
327, 394 
in uremia, 313 
Venous blood-pressure, 23, 27, 140 
cardiac action and, 149 
critical, 26 

effect of drugs on, 358 
effects of alterations of blood- 
pressure on, 58 
estimation of blood flow, sys- 
tolic output by, 171 
Frank and Reh's method, 

142 
Frey's method, 141 
Gartner's method, 140 
Hooker and Eyster's 

method, 142 
Howell's method, 142 
intravenous needle of 
Moritz and Tabora in, 
143 
spring manometers in, 140 
factors influencing, 146 
in infectious diseases, 207 
intra-ocular pressure and, 427 
intravenous injection and, 

150 
in nephritis, 295 
respiration and, 149 
Schott's test of, 163 
Veratrum viride, 356, 398 
Vertigo in vascular crises, 269 
Visceral manipulations and blood-press- 
ure, 404 
Viscosity of blood, 37 

in pregnancy, 309 
and hypertension, 308 
Visual accommodation, blood-pressure 
and, 435 
method of estimation of blood- 
pressure, 108 
Vries-Reilingh's method of estimation 

of arterial tonus, 182 
Von Kries's tachograph, 180 
Von Recklinghausen's formula of blood- 
pressure quotient, 168 



lis 



INDEX 



Von Recklinghausen's sphygmomano- 
meter, 1 L9 
Vomiting, blood-pressure during, 341, 
390 
dangers of, 341 

of pregnancy and U l-pressure, 

120 

W 

W in 1 1 line of adrenal insufficiency, 271 
Widmer's sphygmomanometer, 112 



X-ray radiation over the adrenal 
glands, 334 



Vohimbin, blood-pressure cITect of, 357 



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